Neuro Brain Flashcards
What runs through the cavernous sinus?
CN 3, 4, VI, V2, 6, carotid
How to find central sulcus (~10 ways)
1) pars bracket sign
2) superior frontal sulcus/pre-central sulcus sign-pst end superior frontal sulcus joins pre central sulcus
3) inverted omega (sigmoid hook)-mohot hand
4) bifid posterior central sulcus=posterior CS bifid appearance 85%
5) thin post central gyrus sign-precentral gyrus thicker than post-central gyrus (1.5:1)
6) intraparietal sulcus intersects post-central sulcus
7) midline sulcus sign-most prominent sulcus
Pars marginalis & “pars bracket sign”
aka marginal sulcus, ramps marginalis.
- Posterosuperior extension of cingulate sulcus separating parental lobule from precuneus of parietal lobe on medial surface of cerebral hemispheres.
- landmark for central sulcus (“pars bracket sign”)-sulcus immediately anterior
central sulcus
Frontal vs parietal lobes. Immediately pst to motor strip
homunculus-ACA and MCA territories
ACA=legs
MCA=the rest
How many layers in the hippocampus and how does that affect img?
- Brighter on FLAIR.
Virchow-robins spaces. What/where are they. Significance of enlargement?
- Dilated/fluid filled, pial lined perivascular spaces that accompany perforating vessels. Contain interstitial fluid (not CSF). Normal variant, very common.
- locations: lenticulostriate a’s (lower 1/3 bg), centrum semiovale, midbrain
- enlargement-mucopolysaccharidoes (Hurles, Hunters), “gelatinous pseudocysts” in cryptococcal meningitis, advanced age atrophy
Cavum variants
1) Septum pellucidum- ant to foramen of monroe, btw FH. 100% preterm (15% adults); rarely causes hydro
2) Cavum vergae- SP + pst extension (pst to FOM, btw LV bodies)
3) Cavum velum interpositum- Extension of quadreminal plate cistern to foramen of monroe. Seen above 3rd Vt and below fornices.
- splay fornices
- Unrelated to SP but can coexist.
Arachnoid granulation vs venous sinus clot
venous sinus clot= linear (AG=round/oval)
Arachnoid granulations
- projection of arachnoid membrane (villi) into dural sinuses that allow CSF to pass from SAS –> venous system
- in transverse & superior sagittal sinuses
- T2 bright
tentorial notch
separates sup from inf tentorium
major anatomic components of midbrain
- Ant –> post:
- Cerebral peduncles-WM tracts
- tegmentum- CN nuc (8 from sup coll level, 9 from inf coll level), GM nuc (substantia nigra, red nucleus, periaquaductal grey), WM tracts
- tectum (quadreminal plate-sup (visual pw) & inf colliculi (auditory pw)
- cerebral aquaduct passes btw teg & tectum
- surrounding cisterns: interpeduncular, quadrigeminal, ambient
substantia nigra
pigmented nucleus, through mb from pons –> sub thalamic region. Imp for mvmt
- pars compacta-dopaminergic cells (PD)
- pars reticularis-GABAergic cells
red nucleus
- relay and control station for cerebellar, GP, and CM impulses
- imp for m tone, posture, locomotion
periaquaductal GM
- Surrounds cerebral aqueduct
- Imp in modulation pain, defensive behavior
Pars nervosa-contents?
“nervous guy in front”
-CN9, Jacobson’s nerve (tympanic branch)
Jacobson’s nerve
tympanic branch of cn 9
Pars vascularis
jugular bulb, CN 10, Arnold’s n (auricular branch), CN 11
7Up, COKE Down
orientation of CN 7 to cochlear branch CN 8 in internal auditory canal (IAC)
-superior vestibular branch sup to inferior
ideal sequence to see CN 7 & 8
T2W
What’s in it?-Foramen ovale
CN V3, accessory meningeal artery
What’s in it?-Foramen rotundum
CN V2 (R2V2)
What’s in it?-Superior orbital fissure
CN3, 4, VI, 6
What’s in it?-Inferior orbital fissure
CN VII
What’s in it?-foramen spinosum
middle meningeal artery
What’s in it?-jugular foramen
Pars Nervosa-CN 9
Pars vascularis-jugular bulb, CN 10, 11
What’s in it?- hypoglossal canal
CN 12
What’s in it?- optic canal
CN 2, opthalmic a
What’s in it?- cavernous sinus
CN 3, 4, VI, VII, 6, carotid artery
What’s in it?- IAC
CN 7, 8 (cochlear, super & inf vestibular components.). 7up, coke down
What’s in it?- Meckel cave
trigeminal ganglion
What’s in it?- Dorello’s canal
CN 6, inferior petrosal sinus
Branches of external carotid-Some Attending Physicians Love Fucking Over Poor Medical Students
- superior thyroid
- ascending pharyngeal
- lingual
- facial
- occipital
- pst auricular
- maxillary
- superficial temporal
temporal tap
poking the head-changes waveform for ECA, not for ICA
ICA segments
- C1-cervical. No branches
- C2-petrous
- C3-lacerum
- C4- cavernous
- C5- clinoid
- C6- ophthalmic/supraclinoid
- C7- communicating
At which spinal level does ICA & ECA bifurcate?
C3/4
Meckel/trigeminal cave/cavity
- CSF containing dural-lined pouch in MCF opening from PCF. Invagination into pstlat cavernous sinus on either side sphenoid bone
- houses trigeminal ganglion
- communicates with prepontine and cerebellopontine cisterns
- ICA is medial
ICA segment C1
Cervical.
- No branches
- Atherosclerosis common.
- dissection (spon’t in W, Marfans/ED)–> partial Horner’s, MCA stroke
- retropharyngeal course–> ENT accidental drainage
ICA segment C2
Petrous
- carotid canal
- aneurysms can be surprisingly big (that’s what she said)
ICA segment C3
Lacerum
- crosses petrolingual ligament
- Meckel’s cave exposed via transfacial approach
ICA segment C4
Cavernous
- cavernous carotid fistulas
- HTN induced aneurysms
ICA segment C5
Clinoid
-aneurysm compress optic n –> blindness
ICA segment C6
Ophthalmic/supraclinoid
- common site aneruysms
- “dural ring”
buzzword: origin at the “dural ring”
ICA segment C6/opthalmic/supraclinoid
ICA segment C7
Communicating
-aneurysm –> CN III–> palsy
major branches at terminal portion of ICA
opthalmic, anterior choroidal, pst communicating
CN3 palsy
1) Pcomm
2) apex basilar artery
3) BA junction w/ superior cerebellar/pst cerebral arteries
MC intracranial vascular variant
fetal org PCA
Fetal origin PCA
- PCA supplied by anterior circulation (ie: occipital lobe supplied by ICA) –> large Pcomm (larger than P1)
- pcomm superolateral to CN3 (instead of superomedial)
Persistent trigeminal artery
- persistent fetal connection btw cavernous ICA to basilar
- increased risk aneurysm
- “tau sign”
anastomotic vein of trolard
- superficial middle cerebral vein superior sagittal sinus
- large
- Trolard=Top
anastomotic vein of labbe
- superficial middle cerebral v transverse sinus
- small
- Labbe=Lower
superficial middle cerebral vein
drains to cavernous sinus
superficial and deep intracranial veins
- superficial: superior cerebral v’s, superficial middle cerebral v, superior anastomotic v of trolard & labbe
- deep: basal v of Rosenthal, v of Galen, inf petrosal sinus
Rolandic vein
in central sulcus
what is the relationship btw v of trolard and labbe?
Inverse
basal v’s of rosenthal
deep v’s that pass lateral to midbrain through ambient cistern and drain into v of Galen. Similar course to PCA
Vein of galen
big vein “great” formed via union 2 ICVs
clinical significance of intracranial collateral venous pathways
Dural sinus accessory drainage into extra cranial vein’s.
- regulate T & P
- passage sinus infection/inflammation –> venous sinus thrombosis
MC locations venous gas embolus from peripheral/central IV?
- cavernous sinus=MC
- orbital v, superficial temporal v, frontal venous sinus, petrosal sinus
Concha Bullosa
middle concha pneumatized.
- normal variant
- obstructive if large
Monro-Kellie Hypothesis
head is closed shell composed of 3 major components which remain in equilibrium: brain, blood, csf.
intracranial hypotension
- CSF down –> volume blood increases
- meningeal engorgement (enhancement), distention dural venous sinuses, prominent intracranial vessels, “pituitary pseudo-mass” (enlargement)
idiopathic intracranial hypertension (pseudotumor cerebri)
- Etiology not well understood-making too much CSF or not absorbing it
- ass-hypoTh, Cushings, vit A toxicity
- CSF up –> ventricles slit like, pituitary shrinks (partially empty sella), venous sinuses appear compressed, vertical tortuosity of optic nerves & flattening of pst sclera
- downward displacement bs –> stretching CN 6
- bilateral lateral transverse sinus stenosis MOST SPECIFIC
-rx: csf letting, acetazolaminde, lumboperitoneal shunts.
Categories of hydrocephalus
- “Communicating”- obstructing or non-obstructing. CSF can exit all ventricles. 25% 4th Vt=N
- “non-communicating-obstructing
Where is level of obstruction in obstructive communicating HCP?
- Btw cisterns & arachnoid granulations.
- MCCs-SAH, meningitis (Tb or bacterial), carcinomatous meningitis
Causes of non-obstructive communicating HCP
- brain atrophy (Ex-vacuo)
- NPH
- choroid plexus papilloma
culprits of obstruction at…FOM, aqueduct, 4th Vt
- FOM-colloid cyst
- aqueduct-aqueduct stenosis, tectal glioma
- 4th Vt-pst fossa tumor, cerebellar edema/bleed
What syx is first and most prominent in NPH?
ataxia
is transependymal flow seen more in acute or chronic HCP?
acute
findings/buzzwords NPH
- “out of proportion to atrophy.” “Wet, wacky, wobbly.”
- frontal, temporal horns.
- upward bowing CC
- transependymal flow and/or flow void in aqueduct & 3rd Vt (treated with surgical shunting.)
syndrome of hydrocephalus in the young and middle-aged Adult (SHYMA)
NPH but <40 yr old. Less wet, more headache.
big 4 causes congenital HCP
1) aquaductal stenosis-MC
2) nt defect, usually chiari II
3) arachnoid cysts
4) DW
mcc congenital obstructive HCP
Aqueductal stenosis
Aqueductal stenosis
- Web/diaphgram at aqueduct –> dilated LV, 3rd Vt, normal 4th Vt.
- Macrocephaly, thinning of cortical mantle
- rx- shunting, 3rd ventriculostomy
- “sunset eyes”-upward gaze paralysis
Bickers Adams Edwards syndrome
- AR aqueductal stenosis variant
- male w/ flexed thumbs
Where is a ventricular shunt normally placed?
- proximally-frontal horn just anterior to foramen of mono
- distally-peritoneum, pleura or RA
imaging to evaluate vt shunt
- non con ct, xray
- rapid single-shot T2 sequence
- US/ct distally for fluid collection
- 0.4 mL pertechnetate
causes of vt shunt failure
1) undershunting
2) over shunting
3) infection
4) hydrothorax
5) ascites
Causes of undershunting proximal obstructions
- ingrowth of choroid plexus and particulate debris/blood products (mcc)
- catheter migration
- proximal > distal
causes of undershunting distal obstructions
- psuedocyst
- catheter migration (MC in children)
“slit like vt’s” in setting of vt shunt
-overshunting –> SD hygroma or hematoma (Monroe kelly)
vt shunt failure via infection-timing, cultures & img
- w/i 6 mo’s
- cultures-blood (-), CSF (+)
- DWI = best (debris in Vts/ventriculitis)
- mild enhancement after placement can be normal
- later: loculations–> restricted flow/obstruction –> isolate/trap 4th vt
when do hydrothoraces & ascites matter for vt shunts?
- if symptomatic.
- ascites may cause inguinal hernias, hydroceles via increased abd P
what is vasogenic edema?
Edema tracking through WM via loss of BBB. Tumor, infection, late stage cerebral ischemia, response to steroids
sequelae of subfalcine/cingulate herniation
ACA compression –> infarct
sequelae of descending transtentorial (uncal) herniation
- uncus & hippo through tentorial incisor.
- effacement IL suprasellar cistern 1st
- duret hemorrhages
- CN3 palsy
- kernohan’s notch/phenomenon
Mechanism of duret hemorrhages in downward transtentorial herniation
- compression perforating basilar artery branches
- midline pontomesencephalic junction, cerebellar peduncles
Mechanism of CN3 palsy in downward transtentorial herniation
-compression btw PCA & superior cerebellar artery.
Kernohan’s Notch/phenomenon
- MB on tentorium forms indentation/notch –> IL hemiparesis
- “false localizing sign”
ascending transtentorial herniation
- posterior fossa mass –> upward herniation of vermis
- obstructive hydrocephalus (level of aqueduct)
- “spinning top”-appearance of midbrain from BL compression along pst aspect
- flattening/reversal of quadrigeminal cistern
buzzword: spinning top
Appearance of midbrain in ascending transtentorial herniation from BL compression along pst aspect
cerebellar tonsil herniation
- occurs after downward transtentorial herniation
- in isolation = chiari I
transcalvarial herniation
herniation brain through fracture
osmotic demyelination/central pontine myelinolysis-imaging, earliest change
- T2(+) CENTRAL pons (spares periphery)
- restricted diffusion lower pons-earliest change
- can be extra-pontine (bg, external capsule, amygdala, cerebellum)
pseudobulbar palsy
- Ass w/ osmotic demyelination/central pontine myelinolysis.
- slurred speech, sensitive gag reflex, labile emotional response.
Wernicke encephalopathy-cause, triad, img, rx
- B1 (thiamine) (-)
- triad-1) acute confusion 2)ataxia 3) ophthalmoplegia
- img: T2/FLAIR medial/dorsal thalamus (around 3rd Vt), periaqueductal grey, maxillary bodies, tectal plate
- enhancement mam bodies=classic
- MR spect=lactate
- Rx=thiamine replacement.
Korsakoff psychosis
- memory loss + confabulation + wernickes (acute confusion, ataxia, ophthalmoplegia)
- -> death
- vit b1 (thiamine) (-)
Marchiafava-Bignami-cause, syx’s, img, acute vs chronic findings
- middle aged male malnourished alcoholics
- syx’s-seizure, m rigidity
- necrosis/demyelination cc (body –> gene –> splenium)
- img: swelling/T2 (+) cc
- “sandwich sign”-preference central fbrs, sparing dorsal/ventral fbrs
- chronic- thinned cc + cystic cavities favoring genu & splenium
- acute=swelling –> chronic = atrophy
“sandwich sign”
preferential involvement of central cc fbrs on sagittal img in Marchiafava-Bignami
Direct alcoholic injury
-cerebellar (esp vermis) atrophy
copper and manganese deposition
T1 bright signal in basal ganglia
-seen in: liver dx (w/ or w/o hepatic encephalopathy), TPN, Wilson’s, non-ketotic hyperglycemia (HNK) (often UL)
methanol toxicity
- putaminal T2 bright, ct hyperdensity
- optic n atrophy, hemorrhagic putaminal & subcortical WM necrosis
carbon monoxide
CT hypodense/T2 (+) GP
PRES
posterior reversible encephalopathy syndrome 2/2 auto regulation in setting of acute HTN or CRX
- BL asymm pst vasogenic edema cortical & subcortical WM (parietal, occipital regions).
- DOES NOT RESTRICT
- sup frontal sulcus also common!
post chemotherapy
- methotrexate
1) PRES- “non classic”: bg, bs, cereb; spare occipital lobes
2) leukoencephalopathy-periVt WM BL symm, confluent T2/FLAIR(+)
3) atrophy
4) mineralizing microangiopathy-Ca
5) disseminated necrotizing leukoencephalopathy-severe WM change demonstrating ring enhancement. Classically: leukemia undergoing crx & radiation. Fatal.
post radiation-general changes, time frame, long term sequela
1) high T2/FLAIR/atrophy along radiation portal
2) hemosiderin depot & mineralizing microangiopathy in BG, subcortical WM
- acute (days-wks)-too rare, don’t care
- early delayed (1-6 mo’s)-periVt WM. Reversible
- late delayed (6 mo)- “mosaic”, deep WM. Masslike, expansile. Sparing U-fbrs & cc. Progressive, mostly reversible
long term-vasculopathy (strokes, moya-moya), mineralizing microangiopathy, vascular malformations, cancer (meningioma MC s/p 15 yrs;glioma/sarcoma <10 yrs)
most important risk factor 1˚ CNS neoplasm
radiation
long term sequela s/p radiation
vasculopathy (strokes, moya-moya)
- mineralizing microangiopathy-~2 yrs
- vascular malformations-capillary telangiectasias/cavernous malformations
- cancer (meningioma MC s/p 15 yrs; glioma/sarcoma <10 yrs)
heroin inhalation leukoencephalopathy
- symmetric butterfly in centrum semiovale
- pst limb internal capsule (+)
- deep cerebellar WM (+)
- sparing dentate nucleus
diagnostic criteria for MS
McDonald
1) disseminated in space (periVt, juxtacortical, infratentorial, sc)-> 1 in at least 2 locs
2) dissemination in time: T2(+), enh + T2(+), no enhancement
mc subtype MS
relapsing remitting (85%)
MS trivia- most classic finding, most specific finding, brain atrophy, solitary sc involvement, mc location spine, flair vs T2, MR spec, pediatric specifics, acute plaque features
- most classic finding: T2/FLAIR oval & periVt perpendicular lesions
- calloso-septal interface= 98% (helps differentiate it from vascular lesions & ADEM)
- brain atrophy accelerated
- solitary sc involvement can occur usually with brain lesions
- cervical, peripheral lesions
- FLAIR > T2: juxtacortical and periVt plaques
- T2> FLAIR: infratentorial lesions
- MR spec: NAA (-) in plaques
- acute plaques enhance (partially) + restricted diffusion
ADEM (acute disseminated encephalomyelitis)
- multiple large T2 bright lesions that enhance in nodular or ring pattern
- DO NOT INVOLVE CALLOSO-SEPTAL INTERFACE
Acute hemorrhagic leukoencephalitis (Hurst Disease)
Fulminant form of ADEM with massive swelling & death. Hemorrhage only seen on autopsy (not img).
Devics/neuromyelitis optica
transverse myelitis + optic neuritis.
Marburg variant
- aka acute, fulminant or malignant MS
- childhood MS variant
- death w/i 1 yr from involvement bs or ME w/ herniation
- febrile prodrome
- MR: extensive confluent areas of tumefactive demyelination w/ mass effect
subcortical arteriosclerotic encephalopathy (SAE)
aka Binswanger Disease
- HTN, older people
- multi-infarct dx of WM centrum semiovale. Spares U fbrs
CADASIL
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts & Leukoencephalopathy
- MC hereditary stroke disorder. NOTCH3 mutation chromosome 19
- < 40 yrs + migraine + strokes
- multi-infarct WM in FL, TL (classic). OLs spared
motor strip preserved on FDG/PET in which dementia?
degenerative
RFs alzheimer
age, DS
classic features alzheimers
- hippocampal atrophy (1st, most prom)
- lower pst temporoparietal atrophy >3mm (>65%)
buzzwords: “headphones” or “ear muffs”
Alzheimer FDG pattern: low posterior temporoparietal uptake
Amyloid binding tracer
11C PiB (Pittsburgh compound B). Dx Alzheimer
multi-infarct dementia aka
vascular dementia
RFs Multi-infarct dementia
hyperchol, htn, smoking, CADASIL
classic features multi-infarct dementia
cortical & lacunar infarcts. Advanced atrophy. No lobe specificity.
*could knock out motor strip
Picks Dementia AKA, classic features
Frontotemporal dementia.
- AD; 40-50s
- compulsive/inappropriate behaviors=being a PRICK
- severe symmetric atrophy of FL > TL
dementia with lewy bodies-cause, triad
- alpha synuclein, synucleinopathy
- triad: 1) visual halls 2) spon’t PD 3) flucuating ab to concentrate/stay alert
- vs PD: dementia –> motor
dementia with lewy bodies-classic img features
- mild generalized atrophy
- vs AD: hippocampi in tact & spares mid pst cingulate gyrus (“cingulate island sign”)
- FDG(-) in lateral OL
dementia with lewy bodies-classic img features
- mild generalized atrophy.
- FDG(-) in low lateral OL
- vs AD: hippocampi in tact & spares mid pst cingulate gyrus (“cingulate island sign”)
Fahr Diese (syndrome)/BL Striatopallidodentate Calcinosis/1˚ Familial Brain Ca
BG, thal Ca
-Globus typically involved first
Hallervorden Spaz/PKAN (pantothenate kinase associated neuropathy)
Fe in GP
- T2 dark w/ central high signal via necrosis (“eye of the tiger”
- no enh, no restricted diffusion
Amyotrophic Lateral Sclerosis
- Upper motor neuron loss in brain & spine.
- T2/FLAIR rarely (+) in pst int capsule
- Motor band sign on GRE/SWI
cortico-basal degeneration
tauopathy
- “alien limb phenomenon” (50%)
- asymmetric FP atrophy
MELAS syndrome
mitochondrial disorder: LA, Seizures, Stroked
- (+) lactate doublet at 1.3 ppm
- non vascular GM strokes usually in OL, PL
MELAS syndrome
- mitochondrial disorder: LA, Seizures, Strokes
- non-vasc PO GM
- (+) lactate doublet at 1.3 ppm, (-) NAA
- “migrating infarcts”
Leigh Disease
- mitochondrial d.o.
- T2/FLAIR (+) in bs, bg, cerebral peduncles
- can restrict, don’t enh
- (+) lactate doublet at 1.3 ppm
Leigh Disease/Subacute Necrotizing Encephalo-Myelopathy
- mitochondrial d.o.
- GM: bs, bg, cerebral peduncles, periaquaductal. WM: subcortical.
- can restrict, don’t enh
- (+) lactate doublet at 1.3 ppm
Parkinson Disease
-decreased dopaminergic input to (?+ Fe depo in) pars compact of substantial nigra
-DAT Scan-Ioflupane 123: period-shaped putamen
-mild midbrain volume loss w/ butterfly pattern
?-HY: sparing of midbrain and superior cerebellar peduncles
Period-shaped putamen on DAT Scan-Ioflupane 123
Parkinsonism syndrome-PD, MSA, PSP
multiple system atrophy (MSA)
- PD Plus…
- highest yield- cerebellar subtype MSA-C: peduncle atrophy w/ shrunken flat pons + enlarged 4th Vt + “hot cross bun sign” (loss of transverse fbrs).
- I-123 MIBG PD vs MSA (cardiac:mediastinal ratio N in MSA)
progressive supra nuclear palsy (PSP)/Steele-Richardson-Olszewski
- PD Plus (MC)…
- tauopathy
- micky mouse sign-tegmentum atrophy, sparing tectum + peduncles
- hummingbird sign- mb volume loss w/ concave upper surface relative to pons
Wilson disease-What? MC CT & MR findings? Other img findings?
AR hepatic Cu metabolism malfunction –> depo in brain
- “keyser-fleischer rings” (95%)
- MC CT finding-cortical atrophy
- MC MR finding-T1 Bright BG
- T1 & T2 (+) BG, T2(+) dorsal medial thalamus
- panda sign-T2 (+) tegmentum, N dark red nuc & SN
Deep brain stimulators-what are they used to treat? Electrode placement?
- Rx for PD, essential terror, chronic pain
- electrodes in sub thalamic nucleus w/ tips 9 mm from midline (just inside upper most margin of cerebral peduncle)
hunter’s angle
-line connecting tips of spec peaks, should be 45˚, choline –> Cr –> NAA (alphabetically in increasing order)
MR spec: lipid
necrosis
MR spec: lactate
anaerobic metabolism
- N in 1st hr life
- intermediate TE (~140): inversion lactate peak to fix lactate & lipid peak superimposed
MR spec: alanine
amino acid in meningioma
MR spec: N-acetylaspartate (NAA)
neuronal marker
- super high in canavans
- higher glial tumor grade, lower NAA
MR spec: glutamine
- nt
- (+) w/ hepatic encephalopathy (losing the GLU of your brain!)
MR spec: Cr
energy metabolism
-(-) in tumor necrosis
MR spec: Choline (Co)
cell membrane turnover
MR spec: myoinositol (mI)
cell volume regulator & byproduct glc metabolism
- (+)-low grade glioma, AD, PML
- (-)-other dementias, high grade gliomas, hepatic encephalopathy
Demyelinating vs dysmyelinating
- demyelinating-destroys normal myelin
- dysmyelinating- disrupts formation & t.o. myelin
leukodystrophy
fucked WM in a kid 2/2 lysosomal storage, peroxisomal function or mitochondrial dysfunction
Adrenoleukodystrophy (ALD)
- x-linked peroxisomal enzyme deficiency
- parieto-occipital predominance
- “extends across selenium of cc”
- can enhance, restrict
Metachromatic
- MC leukodystrophy
- frontal predominant
- tigroid pattern-periVt, deep WM
- u-fbrs spared
MC leukodystrophy
metachromatic
Alexander Disease
- frontal predominant +/ cerebellum & middle cerebellar peduncle
- can enhance
Canavan Disease
- diffuse BL subcortical U fbrs (“subcortical predominance”)
- elevated NAA
Krabbe
- centrum semiovale & periVt WM PO predominance
- high density foci in CT (thalamus, caudate, deep WM
- early sparing U fbrs
Pelizaeus-Merzbacher
total loss of normal myelination w/ extension to u fbrs
- tigroid (but more classic with metachromatic)
- no enh, no RD
head size: ALD, Metachromatic, Alexander, Canavan, Krabbe, Pelizaeus-Merzbacher, Leigh
- Alex & Canavan: big
- Krabbe: small
- the rest N
TORCH
CMV (mc), toxo (2nd MC), rubella, HSV
CMV
- periVt Ca + polymicrogyria
- targets germinal matrix
toxo
- cats
- BG Ca + hydro
- f (+) in 3rd TM but only causes in 1st 2
rubella
- WM vasculopathy/ischemia (T2+)
- fewer Ca
HSV-2
- endothelial cells–> thrombus/hemorrhagic infarct –> emcephalomalacia, atrophy (hydranencephaly)
- unlike adults, doesn’t not primarily target limbic system
neonatal HIV
- FL atrophy
- faint BG enhancement precedes BG Ca
HIV encephalitis
- 50% aids patients
- CD4 <200
- T2+ symmetric deep WM, spares cortical U fbrs, T1 N
Progressive MF leukoencephalopathy (PML)
- JC virus
- CD4 <50
- CT & T1 (-) single or MF asymmetric lesions & involvement cortical U fbrs
- buzzword: “T2/FLAIR (+) out of proportion to ME”
BW: “T2/FLAIR (+) out of proportion to ME”
Progressive MF leukoencephalopathy (PML)
CMV
- Atrophy,
- periVt hypodensities/T2/FLAIR (+)
- thin ependymal enhancement
cryptococcus meningitis
- mc fungal infection in AIDS.
- basilar meningitis
1) non-enhancing dilated perivascular spaces filled with mucoid gelatinous debris,
2) cryptococcoma- T1 (-), T2 (+) lesions in BG, may ring enhance
toxoplasma meningitis
MC opportunistic infection in AIDS
- ring enhancing lesions (>1cm) + LOTS of edema
- no RD (atypical abscess)
toxoplasma vs lymphoma
- both ring enh
- Toxo=thallium & PET cold, perfusion (-), hem after rx
- Lymphoma= thallium & pet HOT (acts like tumor)
Tb meningitis
- basal cisterns, + obstructive hydroceph
- +/- dystrophic Ca, minimal nodularity
- vasculitis–> infarct (kids)
HSV (1 in adults, 2 in neonates)
- HSV 1-limbic system
- HSV 2- medial temporal lobe (UL or BL) edema; RD restriction-earliest (diffusion > T2 sens)
- spares bg (distinguished from MCA stroke)
- bleeding (adults > kids)
limbic encephalitis
- -paraneoplastic syndroms (from SCLC)
- HSV app, “negative HSV titer”
West Nile
T2+/RD BG + thal.
+/- hem
Creutzfeldt-Jakob Disease-3 imaging appearances
1) RD cortical gyriform-cortex MC early site. +/- BG
2) Hockey stick sgx- BL FLAIR+ dorsal medial thalamus (variant subtype)
3) Pulvinar sgx- BL FLAIR+ pulvinar thalamic nuclei (pst thalamus) (variant subtype)
* rapidly progressive atrophy
Creutzfeldt-Jakob Disease-3 types
1) sporadic (80-90%)
2) variant “mad cow”
3) familial (10%)
neurocysticercosis
- tinea solium. undercooked pork.
- MC locations desc order-SAS, basal cisterns, parenchyma, Vt
- stages: vesicular–> colloidal–> granular–> calcified/involution
Imaging of stages of neurocysicercosis
- stage 1 (vescicular)-cyst + scolex, no enh
- stage 2 (colloidal)-hyperdense cyst, edema + enh
- stage 3 (granular)-early Ca, smaller cysts, less edema/enh
- stage 4 (calcified/involution)- Ca, blooming on SW1
leptomeningeal
pial + arachnoid
pachymeningeal
Dural.
- Does not extend into sulci
- causes: intracranial hypoTN, dural attachment of meningioma, sarcoid, Tb, Wegener’s, fungal infection.
- breast & prostate cancer both deposit solitary dural mets
very testable trivia re: infants & meningitis
sterile reactive subdural
Rim Phoma
2˚ CNS lymphoma is often extra-axial and can be dural based or fill the subarachnoid space
empyema
- Subdural > epidural, (+) complications.
- MCC=frontal sinusitis
- Follow same rules.
intracranial abscess
~<10mm
- ring smooth, thicker on O2/GM side, thinner toward WM,
- vs tumor-irregular ring, large
abscess-hematog vs direct
hematog > direct
cerebritis
early intra-axial inf –> abscess (If not rx)
-vasogenic edema +/-spotty RD
ventriculitis
shunt placement or intrathecal chemo
- fluid fluid levels
- septa–> obstructive hydro
- intraVt abscess extension=deadly
MC loc parenchymal contusion
ant TL * inf FL (scrape rough skull base)
Grading DAI
- grade 1: GW interface
- grade 2: CC
- grade 3: BS
MC locations DAI
- pst cc
- GM/WM FL & TL
imaging DAI
- mult small T2 (+)
- CT often N
SDH vs EDH-“more mass effect than expected for size”
SDH
It Be Iddy Biddy Baby Doo-Doo
- hyper acute <24 hr- T1 Iso, T2 B
- acute (1-3 d’s)- T1 Iso, T2 D
- early SA (>3d)- T1 B, T2 D
- late SA (>7d)- T1 B, T2 B
- Chronic (>14d)- T1 D, T2 D (center may be T2B)
blood on CT-hyperacute acute, acute, SA, chr)
- Hyperacute acute (<1 hr)-hypo
- Acute (1 hr-3 d’s)- hyper
- SA (4d- 3 wk)- prg hypo; peripheral rim enh?
- Chronic (>3 wks)- hypo
Sequelae of SAH
1) hydrocephalus (early)
2) vasospasm (7-10 d)
3) superficial siderosis-late
MCC SAH
Trauma
-saccular aneurysms 2nd MC (MC idiopathic)
Most sensitive MR sequence for SAH. What fake-out to watch out for?
FLAIR (won’t suppress)
-supplemental O2 gives you fake out that looks like SAH on FLAIR
What to think of in setting of atraumatic SAH
1) aneurysm (saccular MC)
2) benign non-aneurysm perimesencephalic hemorrhage
3) superficial siderosis
benign non-aneurysm perimesencephalic hemorrhage
- blood ant to MB & pons (no lateral ext into Sylvia cistern or IHF) without ID’d aneurysm (95%) (ie: CTA negative).
- etiology NWU: venous bleed?
- pts do well-no rebleed or ischemia
superficial siderosis-what is it, classic history and img
- repeated SAH
- “staining on surface with hemosiderin.”
- classic img: gradient low signal coating on surface of brain
- sensorineural hearing loss, ataxia
pseudo-subarachnoid hemorrhage
Diffuse cerebral edema –> 1) diffuse hypo density 2) compression/collapse SAS (hyperdense)
-~40 HU (acute blood=60-70)
Causes intrapenchymal hemorrhage
1) HTN (esp putamen. IV extension)
2) amyloid-dialysis. multiple lobes, different ages
3) SE-numerous small foci RD. BG. surrounding edema, tiny abscesses.
4) other-avm, vasculitis, tumors
Where are SE induced abscesses and mycotic aneurysms usually seen
distal MCA
intraventricular hemorrhage
usual players
ED, SDH causes
- trauma
- dural & high flow AVMs
causes stroke
- ischemia (80%)
- hemorrhagic (20%)
BW: “watershed infarcts in a kid”
moyamoya (idiopathic supraclinoid ICA vasoocclusive disease)
What makes a subacute infarct unique?
Enhances without mass effect
Fogging
A phase in the evolution of stroke when infarcted brain looks like normal tissue as edema improves (2-3 wks)
-classically with non-con CT, also with T2 MRI (IV contrast would demarcate area of infarct)
In what segments of MCA does MCA sign occur?
M1, M2
When does stroke ME peak?
3-5 d’s
Stroke enhancement rule of 3s
starts in 3 days, peaks in 3 wks, gone by 3 mo
artery of percheron
vascular variant char by solitary trunk from one of two PCAs to feed rostral midbrain and both thalami (usually there are several BL paramedic arteries org from PCAs)
BL paramedian thalamic stroke
artery of percheron
structure affected by recurrent artery of heubner stroke
caudate infarct
artery of heubner
branch off proximal ACA
-can get bagged during Acom aneurysm clipping
cardioembolic stroke appearance
- multiple foci of RD scattered BL along vascular territories
- clinical history=afib, endocarditis
fetal Pcom stroke
infarcts in ant & pst distribution
Stroke restricted diffusion time frame
30 mins-2wks
stroke phase RD (+), FLAIR (-)
hyper acute (<6 hrs)
T1, T2, FLAIR and RD changes throughout stroke.
- 0-6 hrs: RD(+), the rest iso
- 6-24 hrs: T1 (-), T2/F/RD (+)
- 24hrs-1 wk: T1 (-) + bright cortical necrosis, T2/F/RD (+)
Hemorrhage transformation-how often does it occur? What is the typical time period? imaging? who gets it?
- 50%
- 6hrs-4d (24 hr with TPA)
- imaging: 1) GM petechia (90%), 2) hematoma (10%)
- anticoagulation, TPA, embolic strokes (esp large), venous infarcts
predictors of hemorrhagic transformation in TPA
- multiple strokes
- proximal MCA occlusion
- > 1/3 MCA territory
- > 6hr since onset delayed recnalization
- no collateral flow
venous infracts-causes
- venous occlusion-dural sinus or deep cerebral vein
- babies-dehydration
- older children-mastoiditis
- adults-coagulopathy, OCP
MC site venous thrombosis
superior sagittal sinus
How often does associated infarct occur with superior sagittal sinus thrombus?
75%
empty delta sign
venous thrombus on contrast enhanced CT
dense sinus
venous thrombus on non-con CT
RF of venous thrombus
heterogenous RD.
edema patterns arterial vs venous stroke
- arterial= cytotoxic
- venous- vasogenic + cytotoxic
stigmata of chronic venous thrombosis
development of dural AVF +/or (+) CSF P from impaired drainage
ASPECTS
Alberta Stroke Program Early CT Score
- start with 10 pts and lose them based on findings
- MCA, acute ischemia
- > 8: good outcome. <7: may CI TPA
BD aneurysm sites (AM I Bleeding Profusely?)
- branch points, anterior circulation (90%)
- Acomm 35%
- M1/M2 junction 30%
- ICA/Pcomm junction 30%
- basilar tip-3%
- PICA-2%
when do aneurysms rupture?
- size
- pst
- prior SAH
- smoking hx
- F
how do locate ruptured aneurysm (in setting of multiple aneurysms)
- sah/clot
- vasospasm
- size
- irregular focal out pouching “Murphy’s tit”
how often are saccular aneurysms multiple?
15-20%
causes of saccular aneurysms?
- idiopathic via congenital deficiency of internal elastic lamina and tunica media at branch points
- smokers, PCKD, CT dl’s, aortic CoA, NF, FMD, AVMs
aneurysm subtypes
- saccular-branch points, ant circulation
- fusiform-pst circulation
- pedicle aneurysm- artery feeding AVM
- mycotic-distal MCAs
- blister aneurysm=broad based non-branch pt (supraclinoid ICA)
fusiform aneurysm associations
- PAN, CT do’s, syphillis
- pst circulation
- mimic CPA mass
pseudo aneurysm
irregular (often saccular) arterial outpouching at strange/atypical location
-+/- adjacent focal hematoma
traumatic aneurysm
often distal secondary to penetrating trauma or adjacent fracture
mycotic aneurysm
often distal, MC in MCA
-hx=endocarditis, meningitis or thrombophlebitis
blister aneurysm
- broad based at non-branch point
- MC site=supraclnoid ICA
- sneak, angio often negative
infundibular widening
- funnel shaped enlargement at org of Pcomm artery (junction of ICA).
- not a true aneurysm
- no greater than 3 mm
pedicle aneurysm
- aneurysm ass with AVM
- found on feeing artery 15%
- hi risk rupture (higher than avm itself) (high flow)
Aneurysm rupture trivia-rate/yr, treatment threshold,
- > 10mm 1% risk of rupture/yr. Pst circulation higher rate/mm
- 7mm anterior circulation=threshold
maximum bleeding sites for Acom, Pcom, MCA trifurcation, basilar tip, PICA
- Acom: interhemispheric fissure
- Pcom: IL basal cistern
- MCA trifucation-sylvian fissure
- basilar tip-interpeduncular cistern, intraVt
- PICA-pst fossa, intraVt
what MR artifact can show a basilar tip aneurysm?
ghosting/pulsation-look in PED!
normal calcifications
- pineal gland
- habencular-pair of small nuclei located above the thalamus at its posterior end close to the midline
- choroid plexus
- dural Ca
- BG
when do you see brain Ca?
- N structures (PG, habencular, CP, dura, BG)
- TS, SW
- infection: cong CMV, Toxo; neurocystercosis
- cavernoma
- avm
- tumors: OD, ED, AC, GB, Meningioma, CP, OS
Old Elephants Age Gracefully
intracranial tumors that calcify (that people talk about: OD, ED, AC, GB
timing of post SAH vasospasm
4-14 d’s
What does vasospasm look like?
-smooth long segments of stenosis involving multiple vascular territories–> stroke
who gets post SAH vasospasm?
Fisher score: >1 mm or intravt/parenchymal extension
-larger=more risk
The Fisher scale is the initial and best known system of classifying the amount of subarachnoid hemorrhage on CT scans, and is useful in predicting the occurrence and severity of cerebral vasospasm, highest in grade 3 2.
non-SAH causes vasospasm
meningitis, PRES, migraine headache
crescent sign
T1(+) intramural blood in dissection
Associated dissected neck vessels in penetrating vs blunt trauma
- penetrating-carotids
- blunt-vertebrals
NASCET
North American symptomatic carotid endarterectomy Trial
-evaluated extra cranial ICA
- maximum ICA stenosis (A) compared to parallel (non-curved) segment of distal cervical ICA (B)
- formula: (1-A/B) x 100= % stenosis
- CEA >50%
MC systemic vasculitis to involve CNS?
PAN (late finding)
MC collagen vascular disease to involve CNS?
SLE
1˚ CNS vasculitis
1˚ angiitis of CNS (PACNS)
2˚ CNS vasculitis from infection (or sarcoid)
Meningitis (bacterial, Tb, Fungal), SE, Sarcoid
systemic vasculitis with CNS involvement
PAN, Temporal arteritis, Wegeners, Takayasu
CNS vasculitis from systemic disease
cocaine, RA, SLE, Lymes
appearance of CNS vasculitis
- multiple areas of vessel narrowing + dil (beaded)
- focal vascular occlusion
Moya Moya-patho, img, who
- non atherosclerotic stenosis of supraclinoid ICA –> occlusion –> progressive stenosis, enlargement of lenticulostriate a’s (puff of smoke)
- watershed distribution
- sickle cell, NF, radiation, DS
- bimodal age distribution (early childhood: stroke, middle age: bleed)
BW: “puff of smoke”
Moya moya angiographic appearance
Crossed cerebellar diaschiasis (CCD)
- corticopontine-cerebellar pathway connecting cerebral hemisphere to opposite cerebellar hemisphere
- pathway disrupted by tumor, radiation, etc–> decreased metabolism. problem is in the cerebrum!
- cross-crossed appearance of hypo metabolism on FDG-PET
dolichoectasia of basilar artery
widened elongated twisty appearance of basilar artery, probably result of chronic HTN (abN vessel remodeling)
- Smoker criteria for severity: height, laterality
- complications: none, dissection, compression CNs, stroke, HCP
Things that RD
- stroke
- bacterial abscess, cjd, herpes
- epidermoids, hyper cellular brain tumors (lymphoma)
- acute MS lesions
- oxyhemoglobin
- post ictal states
- artifacts (susceptibility and t2 shine through.)
Why do things enhance in the brain?
1) extra-axial
2) break down BBB
Signs of extra-axial location.
1) CSF Cleft-one of most reliable.
2) displaced subarachnoid vessels-interposed btw mass & brain. Vessels=flow voids.
3) cortical GM btw mass & WM
4) Displaced, expanded SAS
5) broad dural base/tail
6) bony reaction
how to differentiate btw mets and infection?
infection RD
MC location metastasis for adult vs kid
- adult-supratentorial GW junction (blood flow)
- kids- neuroblastoma (bones, dura, orbit-not brain!)
common met morphology
round, spherical
% mets solitary vs multiple?
25-50%/50%
Bleeding mets-MR CT
melanoma, renal, carcinoid/choriocarcinoma, thyroid
MC intra-axial mass in adult
met (next step: look for primary)
met vs 1˚re: edema
met more edema
1˚ brain tumors that like to be multiple
- lymphoma, multicentric GBM, gliomatosis cerebri
- from seeding: MB, Epend, GBM, Oligodendroglioma
Syndromes associated with tumors
*tumors in syndromes more likely to be MF
1) NF1-optic gliomas, astrocytomas/gbms
2) NF2-BL schwannomas, meningiomas, ependymomas, dermoid cysts
MSME: multiple schwannomas, meningiomas, ependymomas
3) TS-subependymal tubers, IV giant cell astrocytoma
4) VHL-hemangioblastomas (brain, retina)
5) Nevoid basal cell syndrome (Gorlin)-MB
6) Turcot-GBM, MB, Intestinal polyposis
7) Cowdens-lhermitte-duclos (dysplastic cerebellar gangliocytoma)
cortically based tumors
*most intra-axial tumors are in WM. Not much edema (sm ones can be missed.)
-PDOG:
Pleomorphic xanthoastrocytoma (PXA)
Dysembryoplastic Neuroepithelial Tumor (DNET)
Oligodendroglioma
Ganglioglioma
PXA (pleomorphic xanthroastrocytoma)
- peds (10-20 yo)
- always supratentorial, TL
- cyst w/ nodule (50%)
- Enh. No peritumoral T2. Dural tail. Invades leptomeninges
- just like DNET but not an infant
DNET (dysembryoplastic neuroepithelial Tumor)
- hx: seizure resistant to drugs. <20 yo
- TL
- focal cortical dysplasia-80%
- CT-hypodense
- MR: T2 (+) BUBBLY w/ bright FLAIR rim
- bright rim sign: persistent rim of FLAIR signal
Oligodendroglioma
- grade II presenting as slow-growing cortical/subcortical mass (vs other gliomas that mainly off WM)
- 40-50 yo
- FL
- Ca 90% (“ribbon Ca.”) Enh. EXPANDS CORTEX.
- 1p/19q deletion
Ganglioglioma
- any age (13 yr old w/ seizures)
- anywhere (usually TL)
- look like anything (cystic &. solid + focal Ca). Enh. Not bubbly.
intraVt tumors
- From wall/sp:
- ependymoma
- MB
- SEGA
- SubEpend
- central neurocytoma
- from CP
- CP papilloma
- CP carcinoma
- Xanthogranuloma
- Misc
- mets
- meningioma
- colloid cyst
Ependymoma-what, who, where, img
-intraVt tumor w/ bimodal (larger peak ~6 yo)
- 2 flavors:
1) floor of 4th Vt (70%)-toothpaste (For of Luschka/Magendie–> basal cisterns)
2) Sup Tent (30%)-big, >4 cm
-enhance heterogeneous, Ca 50%
Medulloblastoma
- PNET tumor. MC
- bimodal (large peak ~10 yo)
- roof 4th vt –> into 4th vt, no basal cistern effacement
- hyerpdense, enh homog, Ca 20%, RD+
- met fvia CSF (drop mets + Zuckerguss/leptomeningeal enh)
BW: zuckerguss
German for “sugar icing”, leptomeningeal carcinomatosis seen on post contrast imaging of brain and sc.
What is medulloblastoma ass with?
- Basal cell nevus syndrome (Gorlin syndrome)
- Turcots Syndrome
Gorlin syndrome
- thick dural calcs
- basal cell skin cancer after radiation (ass w/ MB)
- odontogenic cysts
next step if you see pst fossa neoplasm?
preoperative imaging of entire spine
*tumor spread statistically significant predictor of outcome
Subependymal Giant Cell Astrocytoma (SEGA)
- 11 yo TS.
- lateral wall LV (near FOM) –> HCP
- enh homog
SEGA vs Subependymal Nodule (SEN)
SEN stable and found anywhere along lateral Vt. Both calcify.
Subependymoma
- adult
- well circumscribed non enhancing mass in FOM & 4th Vt –> HCP
- T2 (+) (like most tumors)
Central neurocytoma
- most common IV mass in adult (20-40yo)
- “Swiss cheese”-numerous cystic spaces (T2+) + Ca
choroid plexus papilloma
- Peds (85%)-LV trigone. Adults (15%)-4th Vt
- make up ~15% tumors in kids <1yo
Which tumor(s) is the exception to the general rule of thumb that tumors are pst fossa in peds?
choroid plexus origin (Crazy bc reversed)
choroid plexus CA
- only in kids (ie: LV trigone)
- Li-Fraumeni syndrome (p53)
- choroidal arteries shunting blood to tumor on angiography
- +/- CSF dissem (usually solitary)
Xanthogranuloma
adult benign choroid plexus mass
RD+
These lesions represent desquamated epithelium into the lumen of choroid cysts within the choroid plexus. As a result, cholesterol/lipid-rich content of epithelial cells accumulates, sometimes combined with blood products, and results in a xanthomatous response, as this material is ingested by mononuclear cells.
What’s the MC location & 1˚ of intraVt metastasis?
LV trigone (vascular supply of choroid) -Lung (more common in general), but renal goes more often. ie: depends on how question is worded.
colloid cyst
- anterior 3rd vt bind FOM
- img: rounded, hyperdense
- cholesterol: T1+, T2-
- no cholesterol: T2+
mass in LV trigone <10 yo & >40 yo
<10 yo:
choroid plexus papilloma
> 40 yo:
1) met
2) lymphoma
3) meningioma
cerebellar pontine angle masses
1) vestibular schwannoma 75%
2) meningioma 10%
3) epidermoid 5%
is meningioma MC in men or women
women (one of the few)
which tumor may widen the pores acoustics?
schwannoma (trumpet shape, ice cream cone)
which nuc medicine scans are positive in meningioma?
ocreotide & Tc-MDP
what tumor does radiation to the head cause?
meningioma
mc location meningioma
cerebral convexity
meningioma vs schwannoma
- meningioma-enh homog, don’t usually invade IAC, Ca
- schwannoma-enh less homog, invade IAC, less Ca
Causes epidermoid cyst
congenital or acquired (trauma)
MC location dermoid cyst
suprasellar cistern –> pst fossa
*midline (vs epidermoid)
BW “chemical meningitis”
ruptured dermoid.
Ruptured dermoid-MCC, syx’s, and Aunt Minnie appearance ruptured dermoid
- spon’t (MC). Trauma
- headache and seizure
- fat droplets floating in Vts or SAS
arachnoid vs epidermoid cysts
EC=FLAIR (+), RD(+)
Arachnoid cyst
- SAS containing CSF
- (+) in mucopolysaccharidoses
- FLAIR (-), RD (-)
atypical teratoma/rhabdoid tumor (AT/RT)- who, where, img appearance
- WHO IV
- ~2yo
- Cerebellar (can be supratentorial), hetero/necrotic + Ca
medulloblastoma vs atypical teratoma/rhabodid tumor
both WHO grade 4. AT/RT worse
- AT/RT-2 yo; MB 6 yo
- AT/RT Ca, MB doesn’t
BW: “increased head circumference”
Atypical teratoma/rhabdoid tumor
juvenile pilocytic astrocytoma (JPA)
WHO I astrocytoma in kids
- cerebellum > supratentorial
- cyst w/ nodule, nodule & wall enh
- optic tract in NF 1 (pst fossa JPAs not ass with this)
what tumor is the exception that infratentorial tumors are pediatric?
hemangioblastoma
hemangioblastoma-who, where, img, ass
- cerebellar nodule in cyst in ADULT. No wall enh (vs JPA)
- multiple?-von Hippel Lindau
- slowly growing –> HCP
- vascular (peripheral FVs)
- ass w/ poycythemia
what is hemangioblastoma ass with?
- VHL
- polycythemia
diffuse pontine glioma
- 3-10yo, high grade fibrillary glioma in pons
- T2+, subtle/no enh. 4th vt flattened
- img findings= classic –> no biopsy needed
supratentorial adult tumors
astrocytoma, oligodendroglioma (better prognosis)
-IDH mutation
astrocytoma subtypes
-Grade 1 (SEGA, pilocytic astrocytoma)
-grade 2 (low grade astrocytoma, gliomatosis cerebri) (diffuse)- Diffuse T2 at site of tumor, ME, ø enh
-grade 3 (anaplastic): T2/FLAIR mismatch sgx. mild enh.
- grade 4 (GBM): ring & heterog enh. T2/FLAIR+. cross midline
- IDH+ 10%: younger, better prognosis, 2˚ (from progression of previous lower grade)
-IDH(-): older, worst prognosis, 1˚
- IDH+ 10%: younger, better prognosis, 2˚ (from progression of previous lower grade)
ribbon pattern calcification
oligodendroglioma
WHO grade classification. Which tumors are the exception?
- grade 2- low grade, no enh
- grade 3-mild int
- grade 4- intense enh
- exception Pilocytic astrocytoma (enhancing nodule), SEGA (bc IVt)
GBM associations
- Turcot syndrome (GI polyps)
- NF 1
- Li Fraumeni syndrome
T2/FLAIR mismatch sign
T2 bright, FLAIR iso (only a bright rim)
Astrocytoma grades 2 & 3.
Grade 2 astrocytoma
“Diffuse”
- prefers WM
- T2/FLAIR mismatch sgx (bright on T2, hypo on FLAIR)
- no enh
Grade 3 astrocytoma: name, img
“anaplastic”
- prefer WM
- T2/FLAIR mismatch sgx
- mild enh
Grade 4 Astrocytoma
“GBM”
- prefers deep WM
- ring & heterog enh
- T2/FLAIR+
- cross midline. 25% MF
- central locations (like thalamus) worse than normal
- IDH+ 10%: younger, better prognosis, 2˚ (from progression of previous lower grade)
- IDH(-): older, worst prognosis, 1˚
gliomatosis cerebri
diffuse low grade glioma
- at least 3 lobes, BL
- blurring GW differentiation on CT
- T2++
- no enh (low grade)
met vs GBM
- met: irregular ring enh, MF > UF, GWM junction
- GBM: spherical ring enh, UF > MF, deep WM
1˚ lymphoma-types (HL vs NHL), who, ass (virus), img
- non-hodgkin bcell in end-stage AIDS, post transplant.
- EBV+
- intensely enhancing homogenous solid mass in periVt region (“rim phoma”), RD+, thallium+, PET+
“rim phoma”
- Thick, irregular periventricular/ependymal enhancement seen in lymphoma
- vs ependymitis (ex: CMV)-thin, smooth & linear
desmoplastic infantile ganglioglioma/astroctyoma “DIG”
- who 1; -<1 yo
- large, cystic + hydro
- always supratentorial (FL, PL)
supratentorial tumors in peds
DNET
PXA
DIG
BW: rapidly increasing head circumference
desmoplastic infantile ganglioglioma
chordoma
- locally aggressive notochord tumor of midline
- sacrum > clivus > C2 (–> ds –> adj VB)
- T2+
T1
intermediate to low-signal intensity
small foci of hyperintensity (intratumoral hemorrhage or a mucus pool)
T2: most exhibit very high signal
T1 C+ (Gd)
heterogeneous enhancement with a honeycomb appearance corresponding to low T1 signal areas within the tumor
greater enhancement has been associated with poorer prognosis 11
SWI/GE: variable intralesional hemorrhage, suggested by the presence of blooming artefact
DWI/ADC
conventional chordoma: 1474 ± 117 x 10-6 mm2/s 13
dedifferentiated chordoma: 875 ± 100 x 10-6 mm2/s 13
chondrosarcoma
- lateral
- T2(+) + arcs & rings
hemangiopericytoma
soft tissue sarcoma that can mimic aggressive meningioma (bc both enhance homog) BUT no Ca or hyperostosis
-does invade skull.
pituitary adenoma-, what pt of pit, img
- adults (97%). More syx’s in women
- micro <10mm, form in adenohypophysis (ant 2/3). Macro >10mm
- T1/T2 (-), takes up contrast slowly (enh less than N pituitary)
pituitary apoplexy-causes, img, mx
- hemorrhage or infarction of pituitary into enlarged gland (2/2 pregnant or macro adenoma)
- bromocriptine (PL drugs)
- sheehan syndrome (post party)
- cerebral angiography-T1+ (vs adenoma)
- emergent (low BP)
lesions in sella/parasellar region
- adenoma. (T1/T2 -)
- apoplexy-T1+
- rathke cleft cyst- cystic, ie: T2+
- epidermoid
- craniopharyngioma
rathe cleft cyst-origin, app (enh?)
-ectodermal
-cleft btw ant & pst pituitary
-T2+++
-no enh
craniopharyngioma
a) papillary-10%, adults (Papi for Pappi)
b) adamantinomatous- 90%, (Ad for adol)
papillary craniopharyngioma
- adults (papi for pappi)
- less recurrence (encapsulated)
- along infundibulum
- enh+
- no Ca
adamantinomatous craniopharyngioma
- pediatrics
- Ca
- T1/T2+
- enh+
hypothalamic hamartoma-what/where is it, img, classic hx
Aunt minnie for hamartoma in tuber cinereum (pt of HT btw mamm bodies & optic chasm)
- T1/2 iso, no enh
- classic hx: galactic seizures (precocious puberty MC)
-galactic seizure= rare type of seizure that involves a sudden burst of energy, usually in the form of laughing.
buzzword: “machinery oil”
adamantinomatous craniopharyngioma
pineal region tumors
1) germinoma-MC
2) pineoblastoma
3) pineocytoma
4) pineal cyst
* dorsal Parinaud syndrome-vertical gaze palsy)
Pineal Germinoma
- exclusively boys (suprasellar MC in girls)
- mass w/ fat + Ca (“engulfed Ca”) –> heterosexual T1, T2, variable enh
- hCG–> precocious puberty
pineoblastoma
- occur in kids (vs pineocytoma)
- highly invasive
- hetero, enh+++, expanded Ca pattern
- ass w/ retinoblastoma (“trilateral”)
pineocytoma
- rare in childhood
- well-circumscribed & non-invasive
- more solid (enh+++)
- expanded Ca pattern
pineal cyst
incidental
25% Ca
midline crossing
- GBM, lymhoma
- radiation necrosis
- MS plaque in cc
- meningioma of falx
T1 bright tumors (bc most are dark/intermediate! exc if tumor bled)
-fat-dermoid, lipoma
-melanin-melanoma
-blood-bleeding met/tumor
MRCT-melanoma, renal, chorioCA, thyroid
pituitary apoplexy
-cholesterol- colloid cyst
Lhermitte-Duclos/Dysplastic Cerebellar Gangliocytoma
- hamartoma
- tiger stripe mass in 1 cerebellar hemisphere (occasionally causes vermis)
- associated with Cowdens syndrome & breast cancer–> mammogram
Cowden Syndrome
- aka multiple hamartoma syndrome
- char by multiple hamartomas throughout body & increased risk of several cancers
MC type of high flow vascular malformation
high flow AVM
AVM vs Dural AVF
- AVM is high flow, congenital and has nidus.
- Dural AVF is variable flow, acquired (dural sinus thrombosis) and no nidus.
Symptom of high flow AVM
#1 HA #2 Seizure
Symptom of dural AVF
tinnitus (esp if signmoid sinus involved)
Risk of AVM bleed
- bleeding MC complication (3% annual)
- smaller AVM (higher P)
- smaller draining vein (can’t reduce P)
- perinidal aneurysm
- BG location
Imaging high flow AVM
- supratentorial (usually)
- a –> nidus –> v
- adjacent brain may be gliotic (T2+) & atrophic
- wedge-type configuration is typical
- “pedicle aneurysm”
Imaging dural AVF
- no nidus
- transosseous vascular channels/perforating vess
- can be occult on MRI/MRA-catheter angio if high suspicion
What increases the risk of a dural AVF bleed
direct cortical venous drainage
developmental venous anomaly (DVA)
-how to differ from cavernoma
-what happens if you resect it?
- Congenital variation in normal venous drainage associated with cavernous malformations (never bleed in isolation-if see evidence of prior bleed/blooming on GRE, probably have associated cavernoma)
- resection :( –> venous infarct
imaging DVA
“Caput madusa”-enlarged umbrella like collection of enlarged medullary (WM) v’s
- “Large tree with multiple small branches”
- collection of vessels converging towards enlarged v (seen on venous phase only)
- +/- T2+ gliosis
cavernous malformation/cavernoma/cavernous angioma: what is it, causes
- low flow, benign vascular hamartoma containing immature bv’s and no intervening normal brain tissue; possibly 2/2 radiation
- small ooze, nothing catastrophic. Intralesional bleeds diff ages
imaging cavernoma
- “popcorn-like” with “peripheral rim of hemosiderin”
- locules w/ blood at different stages of evolution (F/F level suggests recent)
- GRE
- +/- associated DVA
- solitary or multiple (mc in hispanics)
- sm or large
capillary telangiectasia-what, cause, sig, common sites, img
- low flow cluster of enlarged, dilated capillaries interspersed with normal brain parenchyma
- can be 2/2 radiation
- incidental. usually don’t bleed.
Imaging
General features
Common sites: Pons, cerebellum, spinal cord
Usually < 1 cm
CT
Usually normal
MR
T1 usually normal
T2
50% normal on T2
50% show faint stippled foci of hyperintensity
Large BCTs may show ill-defined FLAIR hyperintensity
Moderately hypointense on GRE; profoundly hypointense on SWI
T1 C+ shows faint stippled or speckled brush-like enhancement
Large BCTs typically contain prominent linear draining vein(s)
imaging capillary telangiectasia
- brush like, stippled pattern of enhancement
- solitary lesion in the pons
- GRE
Habenular calcification-what, ass
- curvilinear structure e~mm ant to pineal body normally calcified in 1/5 adults.
- trivia: (+) ass w/ schizophrenia
choroid plexus locations
- pia mater
-Roof of 3rd ventricle, body & temporal horn of lateral ventricle via choroidal fissure, inferior roof of 4th ventricle
- all ventricles except F/OLs and cerebral aquaduct.
Is pineal gland calcification common?-what should you think of in kids
In adults. Rare in kids (geminoma, pineoblastoma or pineocytoma)
“Engulfed” Ca pattern of pineal gland
germinoma
“expanded” Ca pattern of pineal gland
pineoblastoma & pineocytoma
name that syndrome: basal cell carcinoma and odontogenic keratocysts
Gorlin Syndrome
What part of BG does Ca favor?
globus pallidus
extensive, symmetric BG Ca
Fahr disease
types of mixed vascular malformations
1) DVA + AV shunt
2) DVA + telangiectasia
bright rim sign
persistent rim of FLAIR signal char of DNET
intracranial vascular anomalies to consider
- AVM
- dural AVF
- cavernous
- developmental venous anomaly
- capillary telangiectasia
vascular malformations with and w/o shunting
- with: AVM, dural AVF, pial AVF, vein of galen aneurysmal malformation
- w/o-developmental venous anomaly, sinus pericranii, cavernous malformation, capillary telangiectasia
AVM grading system
Spetzler Martin
meningeal hemangiopericytoma
aggressive form of solitary meningioma
- large, hetero + dural tail
- stat6 and CD34+
- (+) risk recurrence
MS locations (4 total)
- juxtacortical/intracortical
- periVt
- infratentorial
- spinal cord
multinodular and vacuolating neuronal tumor-where, appearance, pres, who, mx
- Small ‘bubbly’ indolent subcortical tumors
- young/middle-aged adult with new onset seizure
- These tumors have been most frequently identified in the temporal lobe, although that is likely to be due to that location being more likely to result in seizures than necessarily a predilection for that lobe
- type of glioneuronal and neuronal tumors
- T2/FLAIR+, T1-, usually enh(-)
- mx: MVNTs appear to be benign tumors with very indolent biological behavior which can, if asymptomatic, be followed by imaging alone. In symptomatic patients (where the MVNT is causing seizures) surgical resection often controls seizures, with no tumor regrowth reported
