Radiology: Cns Infections - Brain

Front 1

how do pyogenic infections of hte brain spread

Back 1

direct extension, after trauma, surgery, sinusitis
hematogenously

Front 2

in brain, where do infx most often occur in hematogenous spread, and why?

Back 2

MCA distribution, b/c that is the lrgst blood flow territory

Front 3

in brain, where is abscess formation most common

Back 3

GW jxn

Front 4

stages of brain abscess development

Back 4

1. Early cerebritis
2. Late cerebritis
3. Early capsule
4. Late capsule

Front 5

findings of early cerebritis

Back 5

infected portion of brain is swollen, edematous. There are areas of necrosis
Lesion is ill-defined.
Patchy enhancement
findings non-spec.

Front 6

when does late cerebritis occur

Back 6

occurs 1-2 wks post infx

Front 7

Findings of late cerebritis

Back 7

increased central necrosis
increased BV peripherally, with thick irregular contrast enhnancement
High T2/FLAIR and DWI centrally
no discrete capsule

Front 8

Findings of early capsule stage of abscess

Back 8

w/i 2 weeks, the infection is walled off
necrotic cntr
rim low T2, cntr high T2/FLAIR
+vasogenic edema
high DWI centrally

Front 9

apperance of late capsule stage of abscess

Back 9

rim enhancement even more pronounced
iso/high T1, low T2
very very increased restricted diffusion

Front 10

Tx of solitary cerebral abscess

Back 10

Surgery

Front 11

DDx pyogenic abscess in brain

Back 11

tumor
resolving hematoma

Front 12

Appeaerance fo septic emobli

Back 12

often looks like an infarct (unlike abscess, there is no capsule)

Front 13

Complications of septic emboli to brain

Back 13

mycotic aneurysm formation --> IPH or SAH

Front 14

MR appearance of listeria in brain

Back 14

abn sig and enhancement in brainstem and cbl white matter

Front 15

DDx CNS listeria

Back 15

ADEM

Front 16

How does cerebral coccidio present

Back 16

less than 1% --> meningigits
focal parenchymal granulomata formation (rare)

Front 17

how does CNS blastomycosis present

Back 17

meningitis > abscess and granulomata

Front 18

how does cns histo present

Back 18

meningitis and granulomata more common
abscess is rare

Front 19

appearance of fungal granulomata

Back 19

small lesion with solid or thick rim enhancement

Front 20

appearance of fungal meningitis

Back 20

meningeal enhancement

Front 21

how does aspergillosis reach brain

Back 21

hematog seeding or direct extension from paranasal sinus
--> meningitis/encephalitis

Front 22

MR findings of CNS aspergillosis

Back 22

ring enhancing abscess
meningitis/encephalitis
subcortical or cortical infarcts from BV invasion

Front 23

how does mucor spread to brain

Back 23

direct extension most often
occ hematogenously

Front 24

imaging findings of mucor

Back 24

single or mult mass lesions with varying enhancement;
infarct, hemorrhage, meningeal enhancement

Front 25

location of CNS mucor

Back 25

base of brain

Front 26

most common imaging presentation of CNS candida

Back 26

meningitis >>> granulomas, small abscesses

Front 27

most common fungal CNS infx

Back 27

crypto

Front 28

who gets CNS crypto

Back 28

50% have nml immune system
50% immunocompromised

Front 29

spread of crypto from lungs

Back 29

hematogenously from lungs

Front 30

CT appearance of crypto

Back 30

nml most often
10% p/w mass lesion

Front 31

appearance of cryptococcoma

Back 31

small, multiple solid enhancing peripheral parenchymal nodule +/- calcs

Front 32

wahat is the name of the mass lesion occ seen in CNS cryptococcus

Back 32

cryptococcoma

Front 33

MR appearance of cryptococcal meningitis

Back 33

leptomeningeal nodules (seen only post-contrast)
also see small enhancing lesions near basal cisterns and sulci
diffuse meningeal enhancement is rare

Front 34

what is gelatinous pseudocyst

Back 34

cystic lesion in BG = enlarged VR space filled with crypto (seen best on MR)

Front 35

who gets gelatinous pseudocyst

Back 35

immunocompromised

Front 36

what disease is gelatinous pseudocyst assoc w

Back 36

cryptococcus

Front 37

organism of cystercircosis

Back 37

T Solium

Front 38

diff types of cystercircosis
?MC)

Back 38

parenchymal (most common)
intraventricular
meningobasal

Front 39

appearance fo parenchymal cystercircosis

Back 39

early on, CT/MR shows edema and nodular enhancemenet
Later, viable cysts are seen -> small (near GWJ)
+/- scolex
no edema
when cyst dies, fluid leaeks out --> inflammation and acute encephalitis; at this stage there is ring enh lesion and edema

Front 40

most common age of TB meningitis

Back 40

infants and children most frequently

Front 41

imaging findings of TB meningitis, location?

Back 41

enhancing, thickened meninges, esp at BASE of BRAIN

Front 42

how to differnetiate TB and bacterial meningitis on basis of imaging

Back 42

TB meningitis has thickened meninges at base of brain
bacterial meningitis has peripheral thickened meninges

Front 43

Possible complications of meningitis

Back 43

thick exudate enetering VR spaces --> vasculitis --> infarcts
communicating hydrocephalus

Front 44

DDx TB meningitis

Back 44

racemos cystercircosis
sarcoid
carcinomatous meningitis
fungal meningitis

Front 45

appearance of fungal meningitis

Back 45

thick meningeal enhancement of basal cisterns

Front 46

appearance of viral meningitis

Back 46

usually nml

Front 47

appearance cns sarcoid (brain) - location?

Back 47

thick meningeal enhancement of basal cisterns (similar location as TB meningitis)

Front 48

complication of subdural empyema

Back 48

cortical venous thrombosis --> venous infarcts

Front 49

appearance of epidural abscess

Back 49

inwardly convex, extra-axial collection with increased density
inner margin enhances

Front 50

ramsay hunt syndrome

Back 50

Zoster of CN VII --> ear pain, facial paralysis, vesicular eruption by the ear

Front 51

ct/mr appearance of ramsay hunt syndrome

Back 51

CT nml
MR --> increased enhancement of facial nerve

Front 52

mortality rate of herpes encephalitis

Back 52

>70% mortality without tx

Front 53

CT findings of CNS hsv

Back 53

poorly defined area of decreased density, swelling, with mass effect in 1 or both temporal lobes.
frontal and insular cortex can be involved.
putamen usually spared

Front 54

why does herpes encephalitis affect the temporal lobe

Back 54

the virus is latent in the gasserian ganglia

Front 55

age of adult herpes encephalitis

Back 55

>50 yo

Front 56

MR findings of adult herpes encephalitis

Back 56

increased FLAIR in temp lobe +/- frontal and insular cortex
meningeal and parenchymal enhancement
+/- hemorrhage

Front 57

DDx MR appearance of herpes encephalitis

Back 57

MCA infarct (although this usually involves putamen)
early bacterial cerebritis
viral encephalitis

Front 58

presentation of CNS varicella zoster

Back 58

encephalitis
cerebral angiitis
cranial neuritis

Front 59

sequellae of cerebral angiitis 2/2 CNS varicella zoster

Back 59

herpes zoster ophthalmicus and delayed contralateral hemiparesis

Front 60

pathophys of sequella of cerebral angiitis 2/2 CNS varicella zoster

Back 60

lrg and medium BV affected --> infarcts from narrowing and beading of arteries

Front 61

pathophys of ADEM

Back 61

acute demyelinating dz after viral infx , vaccination, or spontaneously

Front 62

findings of ADEM on MR

Back 62

high T2/FLAIR in WM of brainstem, cbl, BG
lesions are usually multiple, but few in #
ring or solid enhancement pattern

Front 63

DDX ADEM

Back 63

MS

Front 64

variant of ADEM

Back 64

acute hemorrhagic leukoencephalopathy

Front 65

appearance of acute hemorrhagic leukoencephalopathy
?location

Back 65

perivascular hemorrhagic necrosis, esp in cso
rapid progression of WM lesions over svl days

Front 66

appearance of west nile virus

Back 66

increased T2 in thalami and BG

Front 67

presentation of rasmussen encephalitis

Back 67

intractable sz
progressive neuro deficits

Front 68

appearance of rasmussen encephalitis

Back 68

severe atrophy of involved hemisphere (only 1 hemisphere is usually involved)

Front 69

types of CJD

Back 69

sCJD ("slow" virus)
vCJD (mad cow diseasE)

Front 70

presentation of symptomatic congential CMV

Back 70

hepatosplenomegaly
jaundice
psychomotor retardation
chorioretinitis
deafness
MR

Front 71

findings assoc with congential CMV

Back 71

depends on GA when infected
1st trimester: necrosis of germinal matrix --> migrational abnormalities, agyria, polymicrogyria, focal cortical dysplasia, delayed myelination; cbl hypoplasia

if later: nml gyral patterns, delayed myelination

all: periventricular calcs

Front 72

pattern of calcifciation in congential CMV

Back 72

Periventricular calcs (most common )

Front 73

prenatal u/s findings of congenital CMV
contrast to another similar dz?

Back 73

PV calcs
unlike toxo, no calcs in bg of cortex

Front 74

presentation of neonatal HSV

Back 74

szs in 2-4 WOL
microcephaly
MR
enlarged vents
multicystic encephalomalacia

Front 75

CT findings of conge HSV

Back 75

low density in cerebral WM and cortex
relative sparing of GB, thalami, and posterior fossa

Front 76

US findings of congen HSV

Back 76

echogenic areas which correspond to low density zones

Front 77

clinical presentation of congen toxo

Back 77

microcephaly
chorioretinitis
MR

Front 78

imaging findings of congen toxo

Back 78

atrophy
dilated vents
calcs in pvwm, bg, and cerebral hemispheres

Front 79

imaging findings that differentiate congen toxo and cmv

Back 79

cmv calcs are only perivent
toxo calcs are pv, bg, and hemispheric

Front 80

clinical findings of neurosyph

Back 80

aseptic meningitis
tabes dorsalis
paresis
meningovasc dz

Front 81

imaging findings of neurosyph

Back 81

gummas (small enhancing nodules at surface of brain w adjacent mening enhancement)

Front 82

how does meningovasc dz present in neurosyph

Back 82

acute stroke syndrome, with small infarcts in \BG, WM, cortex, cbl
patchy gyriform enh

Front 83

which CN are affected by lyme dz

Back 83

CN III-VIII

Front 84

MR findings in lyme

Back 84

multi sm WM lesions with ring like enhancement

Front 85

appearance of late stage cystercircosis

Back 85

multiple calcs in GM and GWJ

Front 86

appearance of intraventricular cystercircosis

Back 86

cystic mass that is slighltly increased in signal to CSF
if scolex present, look for increased signal intensity in scolex as well

Front 87

another name for racemose cystercircosis

Back 87

sub arachnoid cystercircosis
multiple non-enhancing cysts in subarach space

Front 88

early and late MR findings of sCJD

Back 88

early: restricted diffusion in cortex and BG

late: atrophy, increased FLAIR/T2 in cortex and BG

Front 89

MR findigns in vCJD

Back 89

increased T2 in posterior thalamus

Front 90

MC cause of meningitis in children

Back 90

H flu

Front 91

MC cause of meningitis in teens/YA

Back 91

N. meningitidis

Front 92

MC cause of meningitis in older adults

Back 92

S pneumo

Front 93

MC cause of meningitis in neonates

Back 93

GBS
E coli
Listeria

Front 94

CT findings in bacterial meningitis

Back 94

usually nml
occasionally, can have increased density peripherally within subarach space, sim to SAH
occassional cerebral edema

Front 95

complications of bacterial meningitis

Back 95

hydrocepha
cerebritis
abscess
ventriculitis
infarct

Front 96

patholphys of hydroceph in meningitis

Back 96

arachnoid villi are unable to absorb csf well --> communicated hydrocephalus

Front 97

what is subdural effusion associated with

Back 97

H flu esp in babies

Front 98

appearance of subdural effusion

Back 98

subdural clxn isodense to CSF

Front 99

appearance of subdural empyema

Back 99

subdural clxn with enhancing inner margin and restricted diffusion

Front 100

pathology of HIV encephalopathy
what part of brain is most affected

Back 100

vaculoization of WM with demyelination
cso most affected
GM usually spared

Front 101

presentation of HIV encephalopathy

Back 101

subcortical dementia
loss of milestones in kids

Front 102

t or f:
kids wth hiv often get opportunistic infx and CNS tumors

Back 102

false

Front 103

appearance fo HIV encephalopathy in adults

Back 103

central, diffuse atrophy
diffuse pattern of increased signal in deep WM or multiple punctate WM lesions on T2

Front 104

appearance of HIV encephalopathy in kids

Back 104

atrophy + calcs in GB
occ WM calcs

Front 105

pathophys of CNS toxo in HIV

Back 105

toxo gets reactivarted --> nectrotizing encephalitis --> mult thin walled abscesses

Front 106

appearance of HIV encephalopathy in kids

Back 106

atrophy + calcs in GB
occ WM calcs

Front 107

appearance of CNS toxo

Back 107

mult ring enhancing lesions with surrounding vasogenic edema
most oftenin BG, but can be seen in WM and cortex

Front 108

pathophys of CNS toxo in HIV

Back 108

toxo gets reactivarted --> nectrotizing encephalitis --> mult thin walled abscesses

Front 109

DDx cns toxo

Back 109

CNS lymphom a
crypto

Front 110

appearance of CNS toxo
location?

Back 110

mult ring enhancing lesions with surrounding vasogenic edema
most oftenin BG, but can be seen in WM and cortex

Front 111

t or f:
bacterial abscesses are common in AIDS pts

Back 111

false

Front 112

DDx cns toxo

Back 112

CNS lymphom a
crypto

Front 113

t or f:
bacterial abscesses are common in AIDS pts

Back 113

false

Front 114

how to disting CNS toxo from lymphoma

Back 114

response to tx
toxo lesions are smaller and more numerous

Front 115

how to disting CNS toxo from crypto

Back 115

no contrast enhancement in crypto

Front 116

pathophys of PML

Back 116

reactivation of JC virus --> demyelination and necrosis of WM

Front 117

apperance of PML

Back 117

focal lesions of high T2/FLAIR and low T1 within subcortical and deep WM
on CT lesions are low density
lesions can be single or multiple
no mass effet or enhancement

Front 118

Distribution of PML

Back 118

in AIDS pts: any part of brain
in non-AIDS pts: occipital lobes most common

Front 119

DDx PML

Back 119

HIV encephalopathy (more diffuse and less intense on T2)
also, doesn't extend to GWJ

Front 120

most common CNS infx in AIDS

Back 120

CMV

Front 121

appearance of CMV meningoenceph

Back 121

high T2 in PVWM
subependymal contrast enhancement
rarely, p/w ring enh lesions

Front 122

where are lesions in CNS lymphoma

Back 122

centrally located within deep white matter or BG