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122 Cards in this Set

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how do pyogenic infections of hte brain spread
direct extension, after trauma, surgery, sinusitis
hematogenously
in brain, where do infx most often occur in hematogenous spread, and why?
MCA distribution, b/c that is the lrgst blood flow territory
in brain, where is abscess formation most common
GW jxn
stages of brain abscess development
1. Early cerebritis
2. Late cerebritis
3. Early capsule
4. Late capsule
findings of early cerebritis
infected portion of brain is swollen, edematous. There are areas of necrosis
Lesion is ill-defined.
Patchy enhancement
findings non-spec.
when does late cerebritis occur
occurs 1-2 wks post infx
Findings of late cerebritis
increased central necrosis
increased BV peripherally, with thick irregular contrast enhnancement
High T2/FLAIR and DWI centrally
no discrete capsule
Findings of early capsule stage of abscess
w/i 2 weeks, the infection is walled off
necrotic cntr
rim low T2, cntr high T2/FLAIR
+vasogenic edema
high DWI centrally
apperance of late capsule stage of abscess
rim enhancement even more pronounced
iso/high T1, low T2
very very increased restricted diffusion
Tx of solitary cerebral abscess
Surgery
DDx pyogenic abscess in brain
tumor
resolving hematoma
Appeaerance fo septic emobli
often looks like an infarct (unlike abscess, there is no capsule)
Complications of septic emboli to brain
mycotic aneurysm formation --> IPH or SAH
MR appearance of listeria in brain
abn sig and enhancement in brainstem and cbl white matter
DDx CNS listeria
ADEM
How does cerebral coccidio present
less than 1% --> meningigits
focal parenchymal granulomata formation (rare)
how does CNS blastomycosis present
meningitis > abscess and granulomata
how does cns histo present
meningitis and granulomata more common
abscess is rare
appearance of fungal granulomata
small lesion with solid or thick rim enhancement
appearance of fungal meningitis
meningeal enhancement
how does aspergillosis reach brain
hematog seeding or direct extension from paranasal sinus
--> meningitis/encephalitis
MR findings of CNS aspergillosis
ring enhancing abscess
meningitis/encephalitis
subcortical or cortical infarcts from BV invasion
how does mucor spread to brain
direct extension most often
occ hematogenously
imaging findings of mucor
single or mult mass lesions with varying enhancement;
infarct, hemorrhage, meningeal enhancement
location of CNS mucor
base of brain
most common imaging presentation of CNS candida
meningitis >>> granulomas, small abscesses
most common fungal CNS infx
crypto
who gets CNS crypto
50% have nml immune system
50% immunocompromised
spread of crypto from lungs
hematogenously from lungs
CT appearance of crypto
nml most often
10% p/w mass lesion
appearance of cryptococcoma
small, multiple solid enhancing peripheral parenchymal nodule +/- calcs
wahat is the name of the mass lesion occ seen in CNS cryptococcus
cryptococcoma
MR appearance of cryptococcal meningitis
leptomeningeal nodules (seen only post-contrast)
also see small enhancing lesions near basal cisterns and sulci
diffuse meningeal enhancement is rare
what is gelatinous pseudocyst
cystic lesion in BG = enlarged VR space filled with crypto (seen best on MR)
who gets gelatinous pseudocyst
immunocompromised
what disease is gelatinous pseudocyst assoc w
cryptococcus
organism of cystercircosis
T Solium
diff types of cystercircosis
?MC)
parenchymal (most common)
intraventricular
meningobasal
appearance fo parenchymal cystercircosis
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
most common age of TB meningitis
infants and children most frequently
imaging findings of TB meningitis, location?
enhancing, thickened meninges, esp at BASE of BRAIN
how to differnetiate TB and bacterial meningitis on basis of imaging
TB meningitis has thickened meninges at base of brain
bacterial meningitis has peripheral thickened meninges
Possible complications of meningitis
thick exudate enetering VR spaces --> vasculitis --> infarcts
communicating hydrocephalus
DDx TB meningitis
racemos cystercircosis
sarcoid
carcinomatous meningitis
fungal meningitis
appearance of fungal meningitis
thick meningeal enhancement of basal cisterns
appearance of viral meningitis
usually nml
appearance cns sarcoid (brain) - location?
thick meningeal enhancement of basal cisterns (similar location as TB meningitis)
complication of subdural empyema
cortical venous thrombosis --> venous infarcts
appearance of epidural abscess
inwardly convex, extra-axial collection with increased density
inner margin enhances
ramsay hunt syndrome
Zoster of CN VII --> ear pain, facial paralysis, vesicular eruption by the ear
ct/mr appearance of ramsay hunt syndrome
CT nml
MR --> increased enhancement of facial nerve
mortality rate of herpes encephalitis
>70% mortality without tx
CT findings of CNS hsv
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
why does herpes encephalitis affect the temporal lobe
the virus is latent in the gasserian ganglia
age of adult herpes encephalitis
>50 yo
MR findings of adult herpes encephalitis
increased FLAIR in temp lobe +/- frontal and insular cortex
meningeal and parenchymal enhancement
+/- hemorrhage
DDx MR appearance of herpes encephalitis
MCA infarct (although this usually involves putamen)
early bacterial cerebritis
viral encephalitis
presentation of CNS varicella zoster
encephalitis
cerebral angiitis
cranial neuritis
sequellae of cerebral angiitis 2/2 CNS varicella zoster
herpes zoster ophthalmicus and delayed contralateral hemiparesis
pathophys of sequella of cerebral angiitis 2/2 CNS varicella zoster
lrg and medium BV affected --> infarcts from narrowing and beading of arteries
pathophys of ADEM
acute demyelinating dz after viral infx , vaccination, or spontaneously
findings of ADEM on MR
high T2/FLAIR in WM of brainstem, cbl, BG
lesions are usually multiple, but few in #
ring or solid enhancement pattern
DDX ADEM
MS
variant of ADEM
acute hemorrhagic leukoencephalopathy
appearance of acute hemorrhagic leukoencephalopathy
?location
perivascular hemorrhagic necrosis, esp in cso
rapid progression of WM lesions over svl days
appearance of west nile virus
increased T2 in thalami and BG
presentation of rasmussen encephalitis
intractable sz
progressive neuro deficits
appearance of rasmussen encephalitis
severe atrophy of involved hemisphere (only 1 hemisphere is usually involved)
types of CJD
sCJD ("slow" virus)
vCJD (mad cow diseasE)
presentation of symptomatic congential CMV
hepatosplenomegaly
jaundice
psychomotor retardation
chorioretinitis
deafness
MR
findings assoc with congential CMV
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
pattern of calcifciation in congential CMV
Periventricular calcs (most common )
prenatal u/s findings of congenital CMV
contrast to another similar dz?
PV calcs
unlike toxo, no calcs in bg of cortex
presentation of neonatal HSV
szs in 2-4 WOL
microcephaly
MR
enlarged vents
multicystic encephalomalacia
CT findings of conge HSV
low density in cerebral WM and cortex
relative sparing of GB, thalami, and posterior fossa
US findings of congen HSV
echogenic areas which correspond to low density zones
clinical presentation of congen toxo
microcephaly
chorioretinitis
MR
imaging findings of congen toxo
atrophy
dilated vents
calcs in pvwm, bg, and cerebral hemispheres
imaging findings that differentiate congen toxo and cmv
cmv calcs are only perivent
toxo calcs are pv, bg, and hemispheric
clinical findings of neurosyph
aseptic meningitis
tabes dorsalis
paresis
meningovasc dz
imaging findings of neurosyph
gummas (small enhancing nodules at surface of brain w adjacent mening enhancement)
how does meningovasc dz present in neurosyph
acute stroke syndrome, with small infarcts in \BG, WM, cortex, cbl
patchy gyriform enh
which CN are affected by lyme dz
CN III-VIII
MR findings in lyme
multi sm WM lesions with ring like enhancement
appearance of late stage cystercircosis
multiple calcs in GM and GWJ
appearance of intraventricular cystercircosis
cystic mass that is slighltly increased in signal to CSF
if scolex present, look for increased signal intensity in scolex as well
another name for racemose cystercircosis
sub arachnoid cystercircosis
multiple non-enhancing cysts in subarach space
early and late MR findings of sCJD
early: restricted diffusion in cortex and BG

late: atrophy, increased FLAIR/T2 in cortex and BG
MR findigns in vCJD
increased T2 in posterior thalamus
MC cause of meningitis in children
H flu
MC cause of meningitis in teens/YA
N. meningitidis
MC cause of meningitis in older adults
S pneumo
MC cause of meningitis in neonates
GBS
E coli
Listeria
CT findings in bacterial meningitis
usually nml
occasionally, can have increased density peripherally within subarach space, sim to SAH
occassional cerebral edema
complications of bacterial meningitis
hydrocepha
cerebritis
abscess
ventriculitis
infarct
patholphys of hydroceph in meningitis
arachnoid villi are unable to absorb csf well --> communicated hydrocephalus
what is subdural effusion associated with
H flu esp in babies
appearance of subdural effusion
subdural clxn isodense to CSF
appearance of subdural empyema
subdural clxn with enhancing inner margin and restricted diffusion
pathology of HIV encephalopathy
what part of brain is most affected
vaculoization of WM with demyelination
cso most affected
GM usually spared
presentation of HIV encephalopathy
subcortical dementia
loss of milestones in kids
t or f:
kids wth hiv often get opportunistic infx and CNS tumors
false
appearance fo HIV encephalopathy in adults
central, diffuse atrophy
diffuse pattern of increased signal in deep WM or multiple punctate WM lesions on T2
appearance of HIV encephalopathy in kids
atrophy + calcs in GB
occ WM calcs
pathophys of CNS toxo in HIV
toxo gets reactivarted --> nectrotizing encephalitis --> mult thin walled abscesses
appearance of HIV encephalopathy in kids
atrophy + calcs in GB
occ WM calcs
appearance of CNS toxo
mult ring enhancing lesions with surrounding vasogenic edema
most oftenin BG, but can be seen in WM and cortex
pathophys of CNS toxo in HIV
toxo gets reactivarted --> nectrotizing encephalitis --> mult thin walled abscesses
DDx cns toxo
CNS lymphom a
crypto
appearance of CNS toxo
location?
mult ring enhancing lesions with surrounding vasogenic edema
most oftenin BG, but can be seen in WM and cortex
t or f:
bacterial abscesses are common in AIDS pts
false
DDx cns toxo
CNS lymphom a
crypto
t or f:
bacterial abscesses are common in AIDS pts
false
how to disting CNS toxo from lymphoma
response to tx
toxo lesions are smaller and more numerous
how to disting CNS toxo from crypto
no contrast enhancement in crypto
pathophys of PML
reactivation of JC virus --> demyelination and necrosis of WM
apperance of PML
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
Distribution of PML
in AIDS pts: any part of brain
in non-AIDS pts: occipital lobes most common
DDx PML
HIV encephalopathy (more diffuse and less intense on T2)
also, doesn't extend to GWJ
most common CNS infx in AIDS
CMV
appearance of CMV meningoenceph
high T2 in PVWM
subependymal contrast enhancement
rarely, p/w ring enh lesions
where are lesions in CNS lymphoma
centrally located within deep white matter or BG