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radiology > Neuro Brain > Flashcards

Neuro Brain Flashcards

1
Q

What runs through the cavernous sinus?

A

CN 3, 4, VI, V2, 6, carotid

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2
Q

How to find central sulcus (~10 ways)

A

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

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3
Q

Pars marginalis & “pars bracket sign”

A

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
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4
Q

central sulcus

A

Frontal vs parietal lobes. Immediately pst to motor strip

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5
Q

homunculus-ACA and MCA territories

A

ACA=legs

MCA=the rest

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6
Q

How many layers in the hippocampus and how does that affect img?

A
  1. Brighter on FLAIR.
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7
Q

Virchow-robins spaces. What/where are they. Significance of enlargement?

A
  • 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
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8
Q

Cavum variants

A

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.

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9
Q

Arachnoid granulation vs venous sinus clot

A

venous sinus clot= linear (AG=round/oval)

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10
Q

Arachnoid granulations

A
  • projection of arachnoid membrane (villi) into dural sinuses that allow CSF to pass from SAS –> venous system
  • in transverse & superior sagittal sinuses
  • T2 bright
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11
Q

tentorial notch

A

separates sup from inf tentorium

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12
Q

major anatomic components of midbrain

A
  • 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
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13
Q

substantia nigra

A

pigmented nucleus, through mb from pons –> sub thalamic region. Imp for mvmt

  • pars compacta-dopaminergic cells (PD)
  • pars reticularis-GABAergic cells
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14
Q

red nucleus

A
  • relay and control station for cerebellar, GP, and CM impulses
  • imp for m tone, posture, locomotion
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15
Q

periaquaductal GM

A
  • Surrounds cerebral aqueduct

- Imp in modulation pain, defensive behavior

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16
Q

Pars nervosa-contents?

A

“nervous guy in front”

-CN9, Jacobson’s nerve (tympanic branch)

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17
Q

Jacobson’s nerve

A

tympanic branch of cn 9

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18
Q

Pars vascularis

A

jugular bulb, CN 10, Arnold’s n (auricular branch), CN 11

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19
Q

7Up, COKE Down

A

orientation of CN 7 to cochlear branch CN 8 in internal auditory canal (IAC)
-superior vestibular branch sup to inferior

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20
Q

ideal sequence to see CN 7 & 8

A

T2W

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21
Q

What’s in it?-Foramen ovale

A

CN V3, accessory meningeal artery

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22
Q

What’s in it?-Foramen rotundum

A

CN V2 (R2V2)

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23
Q

What’s in it?-Superior orbital fissure

A

CN3, 4, VI, 6

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24
Q

What’s in it?-Inferior orbital fissure

A

CN VII

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25
Q

What’s in it?-foramen spinosum

A

middle meningeal artery

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26
Q

What’s in it?-jugular foramen

A

Pars Nervosa-CN 9

Pars vascularis-jugular bulb, CN 10, 11

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27
Q

What’s in it?- hypoglossal canal

A

CN 12

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28
Q

What’s in it?- optic canal

A

CN 2, opthalmic a

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29
Q

What’s in it?- cavernous sinus

A

CN 3, 4, VI, VII, 6, carotid artery

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30
Q

What’s in it?- IAC

A

CN 7, 8 (cochlear, super & inf vestibular components.). 7up, coke down

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31
Q

What’s in it?- Meckel cave

A

trigeminal ganglion

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32
Q

What’s in it?- Dorello’s canal

A

CN 6, inferior petrosal sinus

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33
Q

Branches of external carotid-Some Attending Physicians Love Fucking Over Poor Medical Students

A
  • superior thyroid
  • ascending pharyngeal
  • lingual
  • facial
  • occipital
  • pst auricular
  • maxillary
  • superficial temporal
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34
Q

temporal tap

A

poking the head-changes waveform for ECA, not for ICA

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35
Q

ICA segments

A
  • C1-cervical. No branches
  • C2-petrous
  • C3-lacerum
  • C4- cavernous
  • C5- clinoid
  • C6- ophthalmic/supraclinoid
  • C7- communicating
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36
Q

At which spinal level does ICA & ECA bifurcate?

A

C3/4

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37
Q

Meckel/trigeminal cave/cavity

A
  • 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
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38
Q

ICA segment C1

A

Cervical.

  • No branches
  • Atherosclerosis common.
  • dissection (spon’t in W, Marfans/ED)–> partial Horner’s, MCA stroke
  • retropharyngeal course–> ENT accidental drainage
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39
Q

ICA segment C2

A

Petrous

  • carotid canal
  • aneurysms can be surprisingly big (that’s what she said)
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40
Q

ICA segment C3

A

Lacerum

  • crosses petrolingual ligament
  • Meckel’s cave exposed via transfacial approach
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41
Q

ICA segment C4

A

Cavernous

  • cavernous carotid fistulas
  • HTN induced aneurysms
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42
Q

ICA segment C5

A

Clinoid

-aneurysm compress optic n –> blindness

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43
Q

ICA segment C6

A

Ophthalmic/supraclinoid

  • common site aneruysms
  • “dural ring”
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44
Q

buzzword: origin at the “dural ring”

A

ICA segment C6/opthalmic/supraclinoid

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45
Q

ICA segment C7

A

Communicating

-aneurysm –> CN III–> palsy

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46
Q

major branches at terminal portion of ICA

A

opthalmic, anterior choroidal, pst communicating

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47
Q

CN3 palsy

A

1) Pcomm
2) apex basilar artery
3) BA junction w/ superior cerebellar/pst cerebral arteries

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48
Q

MC intracranial vascular variant

A

fetal org PCA

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49
Q

Fetal origin PCA

A
  • PCA supplied by anterior circulation (ie: occipital lobe supplied by ICA) –> large Pcomm (larger than P1)
  • pcomm superolateral to CN3 (instead of superomedial)
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50
Q

Persistent trigeminal artery

A
  • persistent fetal connection btw cavernous ICA to basilar
  • increased risk aneurysm
  • “tau sign”
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51
Q

anastomotic vein of trolard

A
  • superficial middle cerebral vein superior sagittal sinus
  • large
  • Trolard=Top
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52
Q

anastomotic vein of labbe

A
  • superficial middle cerebral v transverse sinus
  • small
  • Labbe=Lower
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53
Q

superficial middle cerebral vein

A

drains to cavernous sinus

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54
Q

superficial and deep intracranial veins

A
  • 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
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55
Q

Rolandic vein

A

in central sulcus

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56
Q

what is the relationship btw v of trolard and labbe?

A

Inverse

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57
Q

basal v’s of rosenthal

A

deep v’s that pass lateral to midbrain through ambient cistern and drain into v of Galen. Similar course to PCA

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58
Q

Vein of galen

A

big vein “great” formed via union 2 ICVs

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59
Q

clinical significance of intracranial collateral venous pathways

A

Dural sinus accessory drainage into extra cranial vein’s.

  • regulate T & P
  • passage sinus infection/inflammation –> venous sinus thrombosis
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60
Q

MC locations venous gas embolus from peripheral/central IV?

A
  • cavernous sinus=MC

- orbital v, superficial temporal v, frontal venous sinus, petrosal sinus

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61
Q

Concha Bullosa

A

middle concha pneumatized.

  • normal variant
  • obstructive if large
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62
Q

Monro-Kellie Hypothesis

A

head is closed shell composed of 3 major components which remain in equilibrium: brain, blood, csf.

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63
Q

intracranial hypotension

A
  • CSF down –> volume blood increases
  • meningeal engorgement (enhancement), distention dural venous sinuses, prominent intracranial vessels, “pituitary pseudo-mass” (enlargement)
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64
Q

idiopathic intracranial hypertension (pseudotumor cerebri)

A
  • 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.

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65
Q

Categories of hydrocephalus

A
  • “Communicating”- obstructing or non-obstructing. CSF can exit all ventricles. 25% 4th Vt=N
  • “non-communicating-obstructing
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66
Q

Where is level of obstruction in obstructive communicating HCP?

A
  • Btw cisterns & arachnoid granulations.

- MCCs-SAH, meningitis (Tb or bacterial), carcinomatous meningitis

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67
Q

Causes of non-obstructive communicating HCP

A
  • brain atrophy (Ex-vacuo)
  • NPH
  • choroid plexus papilloma
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68
Q

culprits of obstruction at…FOM, aqueduct, 4th Vt

A
  • FOM-colloid cyst
  • aqueduct-aqueduct stenosis, tectal glioma
  • 4th Vt-pst fossa tumor, cerebellar edema/bleed
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69
Q

What syx is first and most prominent in NPH?

A

ataxia

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70
Q

is transependymal flow seen more in acute or chronic HCP?

A

acute

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71
Q

findings/buzzwords NPH

A
  • “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.)
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72
Q

syndrome of hydrocephalus in the young and middle-aged Adult (SHYMA)

A

NPH but <40 yr old. Less wet, more headache.

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73
Q

big 4 causes congenital HCP

A

1) aquaductal stenosis-MC
2) nt defect, usually chiari II
3) arachnoid cysts
4) DW

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74
Q

mcc congenital obstructive HCP

A

Aqueductal stenosis

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75
Q

Aqueductal stenosis

A
  • 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
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76
Q

Bickers Adams Edwards syndrome

A
  • AR aqueductal stenosis variant

- male w/ flexed thumbs

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77
Q

Where is a ventricular shunt normally placed?

A
  • proximally-frontal horn just anterior to foramen of mono

- distally-peritoneum, pleura or RA

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78
Q

imaging to evaluate vt shunt

A
  • non con ct, xray
  • rapid single-shot T2 sequence
  • US/ct distally for fluid collection
  • 0.4 mL pertechnetate
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79
Q

causes of vt shunt failure

A

1) undershunting
2) over shunting
3) infection
4) hydrothorax
5) ascites

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80
Q

Causes of undershunting proximal obstructions

A
  • ingrowth of choroid plexus and particulate debris/blood products (mcc)
  • catheter migration
  • proximal > distal
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81
Q

causes of undershunting distal obstructions

A
  • psuedocyst

- catheter migration (MC in children)

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82
Q

“slit like vt’s” in setting of vt shunt

A

-overshunting –> SD hygroma or hematoma (Monroe kelly)

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83
Q

vt shunt failure via infection-timing, cultures & img

A
  • 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
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84
Q

when do hydrothoraces & ascites matter for vt shunts?

A
  • if symptomatic.

- ascites may cause inguinal hernias, hydroceles via increased abd P

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85
Q

what is vasogenic edema?

A

Edema tracking through WM via loss of BBB. Tumor, infection, late stage cerebral ischemia, response to steroids

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86
Q

sequelae of subfalcine/cingulate herniation

A

ACA compression –> infarct

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87
Q

sequelae of descending transtentorial (uncal) herniation

A
  • uncus & hippo through tentorial incisor.
  • effacement IL suprasellar cistern 1st
  • duret hemorrhages
  • CN3 palsy
  • kernohan’s notch/phenomenon
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88
Q

Mechanism of duret hemorrhages in downward transtentorial herniation

A
  • compression perforating basilar artery branches

- midline pontomesencephalic junction, cerebellar peduncles

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89
Q

Mechanism of CN3 palsy in downward transtentorial herniation

A

-compression btw PCA & superior cerebellar artery.

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90
Q

Kernohan’s Notch/phenomenon

A
  • MB on tentorium forms indentation/notch –> IL hemiparesis

- “false localizing sign”

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91
Q

ascending transtentorial herniation

A
  • 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
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92
Q

buzzword: spinning top

A

Appearance of midbrain in ascending transtentorial herniation from BL compression along pst aspect

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93
Q

cerebellar tonsil herniation

A
  • occurs after downward transtentorial herniation

- in isolation = chiari I

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94
Q

transcalvarial herniation

A

herniation brain through fracture

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95
Q

osmotic demyelination/central pontine myelinolysis-imaging, earliest change

A
  • T2(+) CENTRAL pons (spares periphery)
  • restricted diffusion lower pons-earliest change
  • can be extra-pontine (bg, external capsule, amygdala, cerebellum)
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96
Q

pseudobulbar palsy

A
  • Ass w/ osmotic demyelination/central pontine myelinolysis.

- slurred speech, sensitive gag reflex, labile emotional response.

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97
Q

Wernicke encephalopathy-cause, triad, img, rx

A
  • 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.
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98
Q

Korsakoff psychosis

A
  • memory loss + confabulation + wernickes (acute confusion, ataxia, ophthalmoplegia)
  • -> death
  • vit b1 (thiamine) (-)
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99
Q

Marchiafava-Bignami-cause, syx’s, img, acute vs chronic findings

A
  • 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
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100
Q

“sandwich sign”

A

preferential involvement of central cc fbrs on sagittal img in Marchiafava-Bignami

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101
Q

Direct alcoholic injury

A

-cerebellar (esp vermis) atrophy

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102
Q

copper and manganese deposition

A

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)

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103
Q

methanol toxicity

A
  • putaminal T2 bright, ct hyperdensity

- optic n atrophy, hemorrhagic putaminal & subcortical WM necrosis

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104
Q

carbon monoxide

A

CT hypodense/T2 (+) GP

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105
Q

PRES

A

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!
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106
Q

post chemotherapy

A
  • 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.
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107
Q

post radiation-general changes, time frame, long term sequela

A

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)

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108
Q

most important risk factor 1˚ CNS neoplasm

A

radiation

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109
Q

long term sequela s/p radiation

A

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)
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110
Q

heroin inhalation leukoencephalopathy

A
  • symmetric butterfly in centrum semiovale
  • pst limb internal capsule (+)
  • deep cerebellar WM (+)
  • sparing dentate nucleus
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111
Q

diagnostic criteria for MS

A

McDonald

1) disseminated in space (periVt, juxtacortical, infratentorial, sc)-> 1 in at least 2 locs
2) dissemination in time: T2(+), enh + T2(+), no enhancement

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112
Q

mc subtype MS

A

relapsing remitting (85%)

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113
Q

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

A
  • 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
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114
Q

ADEM (acute disseminated encephalomyelitis)

A
  • multiple large T2 bright lesions that enhance in nodular or ring pattern
  • DO NOT INVOLVE CALLOSO-SEPTAL INTERFACE
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115
Q

Acute hemorrhagic leukoencephalitis (Hurst Disease)

A

Fulminant form of ADEM with massive swelling & death. Hemorrhage only seen on autopsy (not img).

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116
Q

Devics/neuromyelitis optica

A

transverse myelitis + optic neuritis.

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117
Q

Marburg variant

A
  • 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
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118
Q

subcortical arteriosclerotic encephalopathy (SAE)

A

aka Binswanger Disease

  • HTN, older people
  • multi-infarct dx of WM centrum semiovale. Spares U fbrs
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119
Q

CADASIL

A

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
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120
Q

motor strip preserved on FDG/PET in which dementia?

A

degenerative

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121
Q

RFs alzheimer

A

age, DS

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122
Q

classic features alzheimers

A
  • hippocampal atrophy (1st, most prom)

- lower pst temporoparietal atrophy >3mm (>65%)

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123
Q

buzzwords: “headphones” or “ear muffs”

A

Alzheimer FDG pattern: low posterior temporoparietal uptake

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124
Q

Amyloid binding tracer

A

11C PiB (Pittsburgh compound B). Dx Alzheimer

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125
Q

multi-infarct dementia aka

A

vascular dementia

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126
Q

RFs Multi-infarct dementia

A

hyperchol, htn, smoking, CADASIL

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127
Q

classic features multi-infarct dementia

A

cortical & lacunar infarcts. Advanced atrophy. No lobe specificity.
*could knock out motor strip

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128
Q

Picks Dementia AKA, classic features

A

Frontotemporal dementia.

  • AD; 40-50s
  • compulsive/inappropriate behaviors=being a PRICK
  • severe symmetric atrophy of FL > TL
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129
Q

dementia with lewy bodies-cause, triad

A
  • alpha synuclein, synucleinopathy
  • triad: 1) visual halls 2) spon’t PD 3) flucuating ab to concentrate/stay alert
  • vs PD: dementia –> motor
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130
Q

dementia with lewy bodies-classic img features

A
  • mild generalized atrophy
  • vs AD: hippocampi in tact & spares mid pst cingulate gyrus (“cingulate island sign”)
  • FDG(-) in lateral OL
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131
Q

dementia with lewy bodies-classic img features

A
  • mild generalized atrophy.
  • FDG(-) in low lateral OL
  • vs AD: hippocampi in tact & spares mid pst cingulate gyrus (“cingulate island sign”)
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132
Q

Fahr Diese (syndrome)/BL Striatopallidodentate Calcinosis/1˚ Familial Brain Ca

A

BG, thal Ca

-Globus typically involved first

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133
Q

Hallervorden Spaz/PKAN (pantothenate kinase associated neuropathy)

A

Fe in GP

  • T2 dark w/ central high signal via necrosis (“eye of the tiger”
  • no enh, no restricted diffusion
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134
Q

Amyotrophic Lateral Sclerosis

A
  • Upper motor neuron loss in brain & spine.
  • T2/FLAIR rarely (+) in pst int capsule
  • Motor band sign on GRE/SWI
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135
Q

cortico-basal degeneration

A

tauopathy

  • “alien limb phenomenon” (50%)
  • asymmetric FP atrophy
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136
Q

MELAS syndrome

A

mitochondrial disorder: LA, Seizures, Stroked

  • (+) lactate doublet at 1.3 ppm
  • non vascular GM strokes usually in OL, PL
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137
Q

MELAS syndrome

A
  • mitochondrial disorder: LA, Seizures, Strokes
  • non-vasc PO GM
  • (+) lactate doublet at 1.3 ppm, (-) NAA
  • “migrating infarcts”
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138
Q

Leigh Disease

A
  • mitochondrial d.o.
  • T2/FLAIR (+) in bs, bg, cerebral peduncles
  • can restrict, don’t enh
  • (+) lactate doublet at 1.3 ppm
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139
Q

Leigh Disease/Subacute Necrotizing Encephalo-Myelopathy

A
  • mitochondrial d.o.
  • GM: bs, bg, cerebral peduncles, periaquaductal. WM: subcortical.
  • can restrict, don’t enh
  • (+) lactate doublet at 1.3 ppm
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140
Q

Parkinson Disease

A

-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

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141
Q

Period-shaped putamen on DAT Scan-Ioflupane 123

A

Parkinsonism syndrome-PD, MSA, PSP

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142
Q

multiple system atrophy (MSA)

A
  • 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)
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143
Q

progressive supra nuclear palsy (PSP)/Steele-Richardson-Olszewski

A
  • PD Plus (MC)…
  • tauopathy
  • micky mouse sign-tegmentum atrophy, sparing tectum + peduncles
  • hummingbird sign- mb volume loss w/ concave upper surface relative to pons
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144
Q

Wilson disease-What? MC CT & MR findings? Other img findings?

A

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
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145
Q

Deep brain stimulators-what are they used to treat? Electrode placement?

A
  • 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)

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146
Q

hunter’s angle

A

-line connecting tips of spec peaks, should be 45˚, choline –> Cr –> NAA (alphabetically in increasing order)

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147
Q

MR spec: lipid

A

necrosis

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148
Q

MR spec: lactate

A

anaerobic metabolism

  • N in 1st hr life
  • intermediate TE (~140): inversion lactate peak to fix lactate & lipid peak superimposed
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149
Q

MR spec: alanine

A

amino acid in meningioma

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150
Q

MR spec: N-acetylaspartate (NAA)

A

neuronal marker

  • super high in canavans
  • higher glial tumor grade, lower NAA
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151
Q

MR spec: glutamine

A
  • nt

- (+) w/ hepatic encephalopathy (losing the GLU of your brain!)

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152
Q

MR spec: Cr

A

energy metabolism

-(-) in tumor necrosis

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153
Q

MR spec: Choline (Co)

A

cell membrane turnover

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154
Q

MR spec: myoinositol (mI)

A

cell volume regulator & byproduct glc metabolism

  • (+)-low grade glioma, AD, PML
  • (-)-other dementias, high grade gliomas, hepatic encephalopathy
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155
Q

Demyelinating vs dysmyelinating

A
  • demyelinating-destroys normal myelin

- dysmyelinating- disrupts formation & t.o. myelin

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156
Q

leukodystrophy

A

fucked WM in a kid 2/2 lysosomal storage, peroxisomal function or mitochondrial dysfunction

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157
Q

Adrenoleukodystrophy (ALD)

A
  • x-linked peroxisomal enzyme deficiency
  • parieto-occipital predominance
  • “extends across selenium of cc”
  • can enhance, restrict
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158
Q

Metachromatic

A
  • MC leukodystrophy
  • frontal predominant
  • tigroid pattern-periVt, deep WM
  • u-fbrs spared
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159
Q

MC leukodystrophy

A

metachromatic

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160
Q

Alexander Disease

A
  • frontal predominant +/ cerebellum & middle cerebellar peduncle
  • can enhance
161
Q

Canavan Disease

A
  • diffuse BL subcortical U fbrs (“subcortical predominance”)

- elevated NAA

162
Q

Krabbe

A
  • centrum semiovale & periVt WM PO predominance
  • high density foci in CT (thalamus, caudate, deep WM
  • early sparing U fbrs
163
Q

Pelizaeus-Merzbacher

A

total loss of normal myelination w/ extension to u fbrs

  • tigroid (but more classic with metachromatic)
  • no enh, no RD
164
Q

head size: ALD, Metachromatic, Alexander, Canavan, Krabbe, Pelizaeus-Merzbacher, Leigh

A
  • Alex & Canavan: big
  • Krabbe: small
  • the rest N
165
Q

TORCH

A

CMV (mc), toxo (2nd MC), rubella, HSV

166
Q

CMV

A
  • periVt Ca + polymicrogyria

- targets germinal matrix

167
Q

toxo

A
  • cats
  • BG Ca + hydro
  • f (+) in 3rd TM but only causes in 1st 2
168
Q

rubella

A
  • WM vasculopathy/ischemia (T2+)

- fewer Ca

169
Q

HSV-2

A
  • endothelial cells–> thrombus/hemorrhagic infarct –> emcephalomalacia, atrophy (hydranencephaly)
  • unlike adults, doesn’t not primarily target limbic system
170
Q

neonatal HIV

A
  • FL atrophy

- faint BG enhancement precedes BG Ca

171
Q

HIV encephalitis

A
  • 50% aids patients
  • CD4 <200
  • T2+ symmetric deep WM, spares cortical U fbrs, T1 N
172
Q

Progressive MF leukoencephalopathy (PML)

A
  • JC virus
  • CD4 <50
  • CT & T1 (-) single or MF asymmetric lesions & involvement cortical U fbrs
  • buzzword: “T2/FLAIR (+) out of proportion to ME”
173
Q

BW: “T2/FLAIR (+) out of proportion to ME”

A

Progressive MF leukoencephalopathy (PML)

174
Q

CMV

A
  • Atrophy,
  • periVt hypodensities/T2/FLAIR (+)
  • thin ependymal enhancement
175
Q

cryptococcus meningitis

A
  • 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
176
Q

toxoplasma meningitis

A

MC opportunistic infection in AIDS

  • ring enhancing lesions (>1cm) + LOTS of edema
  • no RD (atypical abscess)
177
Q

toxoplasma vs lymphoma

A
  • both ring enh
  • Toxo=thallium & PET cold, perfusion (-), hem after rx
  • Lymphoma= thallium & pet HOT (acts like tumor)
178
Q

Tb meningitis

A
  • basal cisterns, + obstructive hydroceph
  • +/- dystrophic Ca, minimal nodularity
  • vasculitis–> infarct (kids)
179
Q

HSV (1 in adults, 2 in neonates)

A
  • 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)
180
Q

limbic encephalitis

A
  • -paraneoplastic syndroms (from SCLC)

- HSV app, “negative HSV titer”

181
Q

West Nile

A

T2+/RD BG + thal.

+/- hem

182
Q

Creutzfeldt-Jakob Disease-3 imaging appearances

A

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

183
Q

Creutzfeldt-Jakob Disease-3 types

A

1) sporadic (80-90%)
2) variant “mad cow”
3) familial (10%)

184
Q

neurocysticercosis

A
  • tinea solium. undercooked pork.
  • MC locations desc order-SAS, basal cisterns, parenchyma, Vt
  • stages: vesicular–> colloidal–> granular–> calcified/involution
185
Q

Imaging of stages of neurocysicercosis

A
  • 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
186
Q

leptomeningeal

A

pial + arachnoid

187
Q

pachymeningeal

A

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
188
Q

very testable trivia re: infants & meningitis

A

sterile reactive subdural

189
Q

Rim Phoma

A

2˚ CNS lymphoma is often extra-axial and can be dural based or fill the subarachnoid space

190
Q

empyema

A
  • Subdural > epidural, (+) complications.
  • MCC=frontal sinusitis
  • Follow same rules.
191
Q

intracranial abscess

A

~<10mm

  • ring smooth, thicker on O2/GM side, thinner toward WM,
  • vs tumor-irregular ring, large
192
Q

abscess-hematog vs direct

A

hematog > direct

193
Q

cerebritis

A

early intra-axial inf –> abscess (If not rx)

-vasogenic edema +/-spotty RD

194
Q

ventriculitis

A

shunt placement or intrathecal chemo

  • fluid fluid levels
  • septa–> obstructive hydro
  • intraVt abscess extension=deadly
195
Q

MC loc parenchymal contusion

A

ant TL * inf FL (scrape rough skull base)

196
Q

Grading DAI

A
  • grade 1: GW interface
  • grade 2: CC
  • grade 3: BS
197
Q

MC locations DAI

A
  • pst cc

- GM/WM FL & TL

198
Q

imaging DAI

A
  • mult small T2 (+)

- CT often N

199
Q

SDH vs EDH-“more mass effect than expected for size”

A

SDH

200
Q

It Be Iddy Biddy Baby Doo-Doo

A
  • 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)
201
Q

blood on CT-hyperacute acute, acute, SA, chr)

A
  • 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
202
Q

Sequelae of SAH

A

1) hydrocephalus (early)
2) vasospasm (7-10 d)
3) superficial siderosis-late

203
Q

MCC SAH

A

Trauma

-saccular aneurysms 2nd MC (MC idiopathic)

204
Q

Most sensitive MR sequence for SAH. What fake-out to watch out for?

A

FLAIR (won’t suppress)

-supplemental O2 gives you fake out that looks like SAH on FLAIR

205
Q

What to think of in setting of atraumatic SAH

A

1) aneurysm (saccular MC)
2) benign non-aneurysm perimesencephalic hemorrhage
3) superficial siderosis

206
Q

benign non-aneurysm perimesencephalic hemorrhage

A
  • 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
207
Q

superficial siderosis-what is it, classic history and img

A
  • repeated SAH
  • “staining on surface with hemosiderin.”
  • classic img: gradient low signal coating on surface of brain
  • sensorineural hearing loss, ataxia
208
Q

pseudo-subarachnoid hemorrhage

A

Diffuse cerebral edema –> 1) diffuse hypo density 2) compression/collapse SAS (hyperdense)
-~40 HU (acute blood=60-70)

209
Q

Causes intrapenchymal hemorrhage

A

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

210
Q

Where are SE induced abscesses and mycotic aneurysms usually seen

A

distal MCA

211
Q

intraventricular hemorrhage

A

usual players

212
Q

ED, SDH causes

A
  • trauma

- dural & high flow AVMs

213
Q

causes stroke

A
  • ischemia (80%)

- hemorrhagic (20%)

214
Q

BW: “watershed infarcts in a kid”

A

moyamoya (idiopathic supraclinoid ICA vasoocclusive disease)

215
Q

What makes a subacute infarct unique?

A

Enhances without mass effect

216
Q

Fogging

A

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)

217
Q

In what segments of MCA does MCA sign occur?

A

M1, M2

218
Q

When does stroke ME peak?

A

3-5 d’s

219
Q

Stroke enhancement rule of 3s

A

starts in 3 days, peaks in 3 wks, gone by 3 mo

220
Q

artery of percheron

A

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)

221
Q

BL paramedian thalamic stroke

A

artery of percheron

222
Q

structure affected by recurrent artery of heubner stroke

A

caudate infarct

223
Q

artery of heubner

A

branch off proximal ACA

-can get bagged during Acom aneurysm clipping

224
Q

cardioembolic stroke appearance

A
  • multiple foci of RD scattered BL along vascular territories
  • clinical history=afib, endocarditis
225
Q

fetal Pcom stroke

A

infarcts in ant & pst distribution

226
Q

Stroke restricted diffusion time frame

A

30 mins-2wks

227
Q

stroke phase RD (+), FLAIR (-)

A

hyper acute (<6 hrs)

228
Q

T1, T2, FLAIR and RD changes throughout stroke.

A
  • 0-6 hrs: RD(+), the rest iso
  • 6-24 hrs: T1 (-), T2/F/RD (+)
  • 24hrs-1 wk: T1 (-) + bright cortical necrosis, T2/F/RD (+)
229
Q

Hemorrhage transformation-how often does it occur? What is the typical time period? imaging? who gets it?

A
  • 50%
  • 6hrs-4d (24 hr with TPA)
  • imaging: 1) GM petechia (90%), 2) hematoma (10%)
  • anticoagulation, TPA, embolic strokes (esp large), venous infarcts
230
Q

predictors of hemorrhagic transformation in TPA

A
  • multiple strokes
  • proximal MCA occlusion
  • > 1/3 MCA territory
  • > 6hr since onset delayed recnalization
  • no collateral flow
231
Q

venous infracts-causes

A
  • venous occlusion-dural sinus or deep cerebral vein
  • babies-dehydration
  • older children-mastoiditis
  • adults-coagulopathy, OCP
232
Q

MC site venous thrombosis

A

superior sagittal sinus

233
Q

How often does associated infarct occur with superior sagittal sinus thrombus?

A

75%

234
Q

empty delta sign

A

venous thrombus on contrast enhanced CT

235
Q

dense sinus

A

venous thrombus on non-con CT

236
Q

RF of venous thrombus

A

heterogenous RD.

237
Q

edema patterns arterial vs venous stroke

A
  • arterial= cytotoxic

- venous- vasogenic + cytotoxic

238
Q

stigmata of chronic venous thrombosis

A

development of dural AVF +/or (+) CSF P from impaired drainage

239
Q

ASPECTS

A

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
240
Q

BD aneurysm sites (AM I Bleeding Profusely?)

A
  • branch points, anterior circulation (90%)
  • Acomm 35%
  • M1/M2 junction 30%
  • ICA/Pcomm junction 30%
  • basilar tip-3%
  • PICA-2%
241
Q

when do aneurysms rupture?

A
  • size
  • pst
  • prior SAH
  • smoking hx
  • F
242
Q

how do locate ruptured aneurysm (in setting of multiple aneurysms)

A
  • sah/clot
  • vasospasm
  • size
  • irregular focal out pouching “Murphy’s tit”
243
Q

how often are saccular aneurysms multiple?

A

15-20%

244
Q

causes of saccular aneurysms?

A
  • idiopathic via congenital deficiency of internal elastic lamina and tunica media at branch points
  • smokers, PCKD, CT dl’s, aortic CoA, NF, FMD, AVMs
245
Q

aneurysm subtypes

A
  • 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)
246
Q

fusiform aneurysm associations

A
  • PAN, CT do’s, syphillis
  • pst circulation
  • mimic CPA mass
247
Q

pseudo aneurysm

A

irregular (often saccular) arterial outpouching at strange/atypical location
-+/- adjacent focal hematoma

248
Q

traumatic aneurysm

A

often distal secondary to penetrating trauma or adjacent fracture

249
Q

mycotic aneurysm

A

often distal, MC in MCA

-hx=endocarditis, meningitis or thrombophlebitis

250
Q

blister aneurysm

A
  • broad based at non-branch point
  • MC site=supraclnoid ICA
  • sneak, angio often negative
251
Q

infundibular widening

A
  • funnel shaped enlargement at org of Pcomm artery (junction of ICA).
  • not a true aneurysm
  • no greater than 3 mm
252
Q

pedicle aneurysm

A
  • aneurysm ass with AVM
  • found on feeing artery 15%
  • hi risk rupture (higher than avm itself) (high flow)
253
Q

Aneurysm rupture trivia-rate/yr, treatment threshold,

A
  • > 10mm 1% risk of rupture/yr. Pst circulation higher rate/mm
  • 7mm anterior circulation=threshold
254
Q

maximum bleeding sites for Acom, Pcom, MCA trifurcation, basilar tip, PICA

A
  • Acom: interhemispheric fissure
  • Pcom: IL basal cistern
  • MCA trifucation-sylvian fissure
  • basilar tip-interpeduncular cistern, intraVt
  • PICA-pst fossa, intraVt
255
Q

what MR artifact can show a basilar tip aneurysm?

A

ghosting/pulsation-look in PED!

256
Q

normal calcifications

A
  • pineal gland
  • habencular-pair of small nuclei located above the thalamus at its posterior end close to the midline
  • choroid plexus
  • dural Ca
  • BG
257
Q

when do you see brain Ca?

A
  • N structures (PG, habencular, CP, dura, BG)
  • TS, SW
  • infection: cong CMV, Toxo; neurocystercosis
  • cavernoma
  • avm
  • tumors: OD, ED, AC, GB, Meningioma, CP, OS
258
Q

Old Elephants Age Gracefully

A

intracranial tumors that calcify (that people talk about: OD, ED, AC, GB

259
Q

timing of post SAH vasospasm

A

4-14 d’s

260
Q

What does vasospasm look like?

A

-smooth long segments of stenosis involving multiple vascular territories–> stroke

261
Q

who gets post SAH vasospasm?

A

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.

262
Q

non-SAH causes vasospasm

A

meningitis, PRES, migraine headache

263
Q

crescent sign

A

T1(+) intramural blood in dissection

264
Q

Associated dissected neck vessels in penetrating vs blunt trauma

A
  • penetrating-carotids

- blunt-vertebrals

265
Q

NASCET

A

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%
266
Q

MC systemic vasculitis to involve CNS?

A

PAN (late finding)

267
Q

MC collagen vascular disease to involve CNS?

A

SLE

268
Q

1˚ CNS vasculitis

A

1˚ angiitis of CNS (PACNS)

269
Q

2˚ CNS vasculitis from infection (or sarcoid)

A

Meningitis (bacterial, Tb, Fungal), SE, Sarcoid

270
Q

systemic vasculitis with CNS involvement

A

PAN, Temporal arteritis, Wegeners, Takayasu

271
Q

CNS vasculitis from systemic disease

A

cocaine, RA, SLE, Lymes

272
Q

appearance of CNS vasculitis

A
  • multiple areas of vessel narrowing + dil (beaded)

- focal vascular occlusion

273
Q

Moya Moya-patho, img, who

A
  • 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)
274
Q

BW: “puff of smoke”

A

Moya moya angiographic appearance

275
Q

Crossed cerebellar diaschiasis (CCD)

A
  • 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
276
Q

dolichoectasia of basilar artery

A

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
277
Q

Things that RD

A
  • stroke
  • bacterial abscess, cjd, herpes
  • epidermoids, hyper cellular brain tumors (lymphoma)
  • acute MS lesions
  • oxyhemoglobin
  • post ictal states
  • artifacts (susceptibility and t2 shine through.)
278
Q

Why do things enhance in the brain?

A

1) extra-axial

2) break down BBB

279
Q

Signs of extra-axial location.

A

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

280
Q

how to differentiate btw mets and infection?

A

infection RD

281
Q

MC location metastasis for adult vs kid

A
  • adult-supratentorial GW junction (blood flow)

- kids- neuroblastoma (bones, dura, orbit-not brain!)

282
Q

common met morphology

A

round, spherical

283
Q

% mets solitary vs multiple?

A

25-50%/50%

284
Q

Bleeding mets-MR CT

A

melanoma, renal, carcinoid/choriocarcinoma, thyroid

285
Q

MC intra-axial mass in adult

A

met (next step: look for primary)

286
Q

met vs 1˚re: edema

A

met more edema

287
Q

1˚ brain tumors that like to be multiple

A
  • lymphoma, multicentric GBM, gliomatosis cerebri

- from seeding: MB, Epend, GBM, Oligodendroglioma

288
Q

Syndromes associated with tumors

A

*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)

289
Q

cortically based tumors

A

*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

290
Q

PXA (pleomorphic xanthroastrocytoma)

A
  • 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
291
Q

DNET (dysembryoplastic neuroepithelial Tumor)

A
  • 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
292
Q

Oligodendroglioma

A
  • 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
293
Q

Ganglioglioma

A
  • any age (13 yr old w/ seizures)
  • anywhere (usually TL)
  • look like anything (cystic &. solid + focal Ca). Enh. Not bubbly.
294
Q

intraVt tumors

A
  • From wall/sp:
    • ependymoma
    • MB
    • SEGA
    • SubEpend
    • central neurocytoma
  • from CP
    • CP papilloma
    • CP carcinoma
    • Xanthogranuloma
  • Misc
    • mets
    • meningioma
    • colloid cyst
295
Q

Ependymoma-what, who, where, img

A

-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%

296
Q

Medulloblastoma

A
  • 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)
297
Q

BW: zuckerguss

A

German for “sugar icing”, leptomeningeal carcinomatosis seen on post contrast imaging of brain and sc.

298
Q

What is medulloblastoma ass with?

A
  • Basal cell nevus syndrome (Gorlin syndrome)

- Turcots Syndrome

299
Q

Gorlin syndrome

A
  • thick dural calcs
  • basal cell skin cancer after radiation (ass w/ MB)
  • odontogenic cysts
300
Q

next step if you see pst fossa neoplasm?

A

preoperative imaging of entire spine

*tumor spread statistically significant predictor of outcome

301
Q

Subependymal Giant Cell Astrocytoma (SEGA)

A
  • 11 yo TS.
  • lateral wall LV (near FOM) –> HCP
  • enh homog
302
Q

SEGA vs Subependymal Nodule (SEN)

A

SEN stable and found anywhere along lateral Vt. Both calcify.

303
Q

Subependymoma

A
  • adult
  • well circumscribed non enhancing mass in FOM & 4th Vt –> HCP
  • T2 (+) (like most tumors)
304
Q

Central neurocytoma

A
  • most common IV mass in adult (20-40yo)

- “Swiss cheese”-numerous cystic spaces (T2+) + Ca

305
Q

choroid plexus papilloma

A
  • Peds (85%)-LV trigone. Adults (15%)-4th Vt

- make up ~15% tumors in kids <1yo

306
Q

Which tumor(s) is the exception to the general rule of thumb that tumors are pst fossa in peds?

A

choroid plexus origin (Crazy bc reversed)

307
Q

choroid plexus CA

A
  • only in kids (ie: LV trigone)
  • Li-Fraumeni syndrome (p53)
  • choroidal arteries shunting blood to tumor on angiography
  • +/- CSF dissem (usually solitary)
308
Q

Xanthogranuloma

A

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.

309
Q

What’s the MC location & 1˚ of intraVt metastasis?

A 
LV trigone (vascular supply of choroid)
-Lung (more common in general), but renal goes more often. ie: depends on how question is worded.
310
Q

colloid cyst

A
  • anterior 3rd vt bind FOM
  • img: rounded, hyperdense
    • cholesterol: T1+, T2-
    • no cholesterol: T2+
311
Q

mass in LV trigone <10 yo & >40 yo

A

<10 yo:
choroid plexus papilloma

> 40 yo:

1) met
2) lymphoma
3) meningioma

312
Q

cerebellar pontine angle masses

A

1) vestibular schwannoma 75%
2) meningioma 10%
3) epidermoid 5%

313
Q

is meningioma MC in men or women

A

women (one of the few)

314
Q

which tumor may widen the pores acoustics?

A

schwannoma (trumpet shape, ice cream cone)

315
Q

which nuc medicine scans are positive in meningioma?

A

ocreotide & Tc-MDP

316
Q

what tumor does radiation to the head cause?

A

meningioma

317
Q

mc location meningioma

A

cerebral convexity

318
Q

meningioma vs schwannoma

A
  • meningioma-enh homog, don’t usually invade IAC, Ca

- schwannoma-enh less homog, invade IAC, less Ca

319
Q

Causes epidermoid cyst

A

congenital or acquired (trauma)

320
Q

MC location dermoid cyst

A

suprasellar cistern –> pst fossa

*midline (vs epidermoid)

321
Q

BW “chemical meningitis”

A

ruptured dermoid.

322
Q

Ruptured dermoid-MCC, syx’s, and Aunt Minnie appearance ruptured dermoid

A
  • spon’t (MC). Trauma
  • headache and seizure
  • fat droplets floating in Vts or SAS
323
Q

arachnoid vs epidermoid cysts

A

EC=FLAIR (+), RD(+)

324
Q

Arachnoid cyst

A
  • SAS containing CSF
  • (+) in mucopolysaccharidoses
  • FLAIR (-), RD (-)
325
Q

atypical teratoma/rhabdoid tumor (AT/RT)- who, where, img appearance

A
  • WHO IV
  • ~2yo
  • Cerebellar (can be supratentorial), hetero/necrotic + Ca
326
Q

medulloblastoma vs atypical teratoma/rhabodid tumor

A

both WHO grade 4. AT/RT worse

  • AT/RT-2 yo; MB 6 yo
  • AT/RT Ca, MB doesn’t
327
Q

BW: “increased head circumference”

A

Atypical teratoma/rhabdoid tumor

328
Q

juvenile pilocytic astrocytoma (JPA)

A

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)
329
Q

what tumor is the exception that infratentorial tumors are pediatric?

A

hemangioblastoma

330
Q

hemangioblastoma-who, where, img, ass

A
  • cerebellar nodule in cyst in ADULT. No wall enh (vs JPA)
  • multiple?-von Hippel Lindau
  • slowly growing –> HCP
  • vascular (peripheral FVs)
  • ass w/ poycythemia
331
Q

what is hemangioblastoma ass with?

A
  • VHL

- polycythemia

332
Q

diffuse pontine glioma

A
  • 3-10yo, high grade fibrillary glioma in pons
  • T2+, subtle/no enh. 4th vt flattened
  • img findings= classic –> no biopsy needed
333
Q

supratentorial adult tumors

A

astrocytoma, oligodendroglioma (better prognosis)

-IDH mutation

334
Q

astrocytoma subtypes

A

-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˚
335
Q

ribbon pattern calcification

A

oligodendroglioma

336
Q

WHO grade classification. Which tumors are the exception?

A
  • grade 2- low grade, no enh
  • grade 3-mild int
  • grade 4- intense enh
  • exception Pilocytic astrocytoma (enhancing nodule), SEGA (bc IVt)
337
Q

GBM associations

A
  • Turcot syndrome (GI polyps)
  • NF 1
  • Li Fraumeni syndrome
338
Q

T2/FLAIR mismatch sign

A

T2 bright, FLAIR iso (only a bright rim)

Astrocytoma grades 2 & 3.

339
Q

Grade 2 astrocytoma

A

“Diffuse”

  • prefers WM
  • T2/FLAIR mismatch sgx (bright on T2, hypo on FLAIR)
  • no enh
340
Q

Grade 3 astrocytoma: name, img

A

“anaplastic”

  • prefer WM
  • T2/FLAIR mismatch sgx
  • mild enh
341
Q

Grade 4 Astrocytoma

A

“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˚
342
Q

gliomatosis cerebri

A

diffuse low grade glioma

  • at least 3 lobes, BL
  • blurring GW differentiation on CT
  • T2++
  • no enh (low grade)
343
Q

met vs GBM

A
  • met: irregular ring enh, MF > UF, GWM junction

- GBM: spherical ring enh, UF > MF, deep WM

344
Q

1˚ lymphoma-types (HL vs NHL), who, ass (virus), img

A
  • non-hodgkin bcell in end-stage AIDS, post transplant.
  • EBV+
  • intensely enhancing homogenous solid mass in periVt region (“rim phoma”), RD+, thallium+, PET+
345
Q

“rim phoma”

A
  • Thick, irregular periventricular/ependymal enhancement seen in lymphoma
  • vs ependymitis (ex: CMV)-thin, smooth & linear
346
Q

desmoplastic infantile ganglioglioma/astroctyoma “DIG”

A
  • who 1; -<1 yo
  • large, cystic + hydro
  • always supratentorial (FL, PL)
347
Q

supratentorial tumors in peds

A

DNET
PXA
DIG

348
Q

BW: rapidly increasing head circumference

A

desmoplastic infantile ganglioglioma

349
Q

chordoma

A
  • 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

350
Q

chondrosarcoma

A
  • lateral

- T2(+) + arcs & rings

351
Q

hemangiopericytoma

A

soft tissue sarcoma that can mimic aggressive meningioma (bc both enhance homog) BUT no Ca or hyperostosis
-does invade skull.

352
Q

pituitary adenoma-, what pt of pit, img

A
  • 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)
353
Q

pituitary apoplexy-causes, img, mx

A
  • 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)
354
Q

lesions in sella/parasellar region

A
  • adenoma. (T1/T2 -)
  • apoplexy-T1+
  • rathke cleft cyst- cystic, ie: T2+
  • epidermoid
  • craniopharyngioma
355
Q

rathe cleft cyst-origin, app (enh?)

A

-ectodermal
-cleft btw ant & pst pituitary
-T2+++
-no enh

356
Q

craniopharyngioma

A

a) papillary-10%, adults (Papi for Pappi)

b) adamantinomatous- 90%, (Ad for adol)

357
Q

papillary craniopharyngioma

A
  • adults (papi for pappi)
  • less recurrence (encapsulated)
  • along infundibulum
  • enh+
  • no Ca
358
Q

adamantinomatous craniopharyngioma

A
  • pediatrics
  • Ca
  • T1/T2+
  • enh+
359
Q

hypothalamic hamartoma-what/where is it, img, classic hx

A

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.

360
Q

buzzword: “machinery oil”

A

adamantinomatous craniopharyngioma

361
Q

pineal region tumors

A

1) germinoma-MC
2) pineoblastoma
3) pineocytoma
4) pineal cyst
* dorsal Parinaud syndrome-vertical gaze palsy)

362
Q

Pineal Germinoma

A
  • exclusively boys (suprasellar MC in girls)
  • mass w/ fat + Ca (“engulfed Ca”) –> heterosexual T1, T2, variable enh
  • hCG–> precocious puberty
363
Q

pineoblastoma

A
  • occur in kids (vs pineocytoma)
  • highly invasive
  • hetero, enh+++, expanded Ca pattern
  • ass w/ retinoblastoma (“trilateral”)
364
Q

pineocytoma

A
  • rare in childhood
  • well-circumscribed & non-invasive
  • more solid (enh+++)
  • expanded Ca pattern
365
Q

pineal cyst

A

incidental

25% Ca

366
Q

midline crossing

A
  • GBM, lymhoma
  • radiation necrosis
  • MS plaque in cc
  • meningioma of falx
367
Q

T1 bright tumors (bc most are dark/intermediate! exc if tumor bled)

A

-fat-dermoid, lipoma
-melanin-melanoma
-blood-bleeding met/tumor
MRCT-melanoma, renal, chorioCA, thyroid
pituitary apoplexy
-cholesterol- colloid cyst

368
Q

Lhermitte-Duclos/Dysplastic Cerebellar Gangliocytoma

A
  • hamartoma
  • tiger stripe mass in 1 cerebellar hemisphere (occasionally causes vermis)
  • associated with Cowdens syndrome & breast cancer–> mammogram
369
Q

Cowden Syndrome

A
  • aka multiple hamartoma syndrome

- char by multiple hamartomas throughout body & increased risk of several cancers

370
Q

MC type of high flow vascular malformation

A

high flow AVM

371
Q

AVM vs Dural AVF

A
  • AVM is high flow, congenital and has nidus.

- Dural AVF is variable flow, acquired (dural sinus thrombosis) and no nidus.

372
Q

Symptom of high flow AVM

A 
#1 HA
#2 Seizure
373
Q

Symptom of dural AVF

A

tinnitus (esp if signmoid sinus involved)

374
Q

Risk of AVM bleed

A
  • bleeding MC complication (3% annual)
  • smaller AVM (higher P)
  • smaller draining vein (can’t reduce P)
  • perinidal aneurysm
  • BG location
375
Q

Imaging high flow AVM

A
  • supratentorial (usually)
  • a –> nidus –> v
  • adjacent brain may be gliotic (T2+) & atrophic
  • wedge-type configuration is typical
  • “pedicle aneurysm”
376
Q

Imaging dural AVF

A
  • no nidus
  • transosseous vascular channels/perforating vess
  • can be occult on MRI/MRA-catheter angio if high suspicion
377
Q

What increases the risk of a dural AVF bleed

A

direct cortical venous drainage

378
Q

developmental venous anomaly (DVA)
-how to differ from cavernoma
-what happens if you resect it?

A
  • 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
379
Q

imaging DVA

A

“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
380
Q

cavernous malformation/cavernoma/cavernous angioma: what is it, causes

A
  • 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
381
Q

imaging cavernoma

A
  • “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
382
Q

capillary telangiectasia-what, cause, sig, common sites, img

A
  • 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)

383
Q

imaging capillary telangiectasia

A
  • brush like, stippled pattern of enhancement
  • solitary lesion in the pons
  • GRE
384
Q

Habenular calcification-what, ass

A
  • curvilinear structure e~mm ant to pineal body normally calcified in 1/5 adults.
  • trivia: (+) ass w/ schizophrenia
385
Q

choroid plexus locations

A
  • 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.

386
Q

Is pineal gland calcification common?-what should you think of in kids

A

In adults. Rare in kids (geminoma, pineoblastoma or pineocytoma)

387
Q

“Engulfed” Ca pattern of pineal gland

A

germinoma

388
Q

“expanded” Ca pattern of pineal gland

A

pineoblastoma & pineocytoma

389
Q

name that syndrome: basal cell carcinoma and odontogenic keratocysts

A

Gorlin Syndrome

390
Q

What part of BG does Ca favor?

A

globus pallidus

391
Q

extensive, symmetric BG Ca

A

Fahr disease

392
Q

types of mixed vascular malformations

A

1) DVA + AV shunt
2) DVA + telangiectasia

393
Q

bright rim sign

A

persistent rim of FLAIR signal char of DNET

394
Q

intracranial vascular anomalies to consider

A
  • AVM
  • dural AVF
  • cavernous
  • developmental venous anomaly
  • capillary telangiectasia
395
Q

vascular malformations with and w/o shunting

A
  • with: AVM, dural AVF, pial AVF, vein of galen aneurysmal malformation
  • w/o-developmental venous anomaly, sinus pericranii, cavernous malformation, capillary telangiectasia
396
Q

AVM grading system

A

Spetzler Martin

397
Q

meningeal hemangiopericytoma

A

aggressive form of solitary meningioma

  • large, hetero + dural tail
  • stat6 and CD34+
  • (+) risk recurrence
398
Q

MS locations (4 total)

A
  1. juxtacortical/intracortical
  2. periVt
  3. infratentorial
  4. spinal cord
399
Q

multinodular and vacuolating neuronal tumor-where, appearance, pres, who, mx

A
  • 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

radiology (31 decks)

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