an overview of intracranial infections

1. IMAGINGOFINTRACRANIAL
INFECTIONS
Pradeep
Kumar

2. •Congenital / neonatal
infections
•Meningitis
•Pyogenic parenchymal
infections
•Encephalitis
•Tubercular and fungal
infections

3. Congenital/neonatal infections
Causative agents-
1. TORCH agents-Toxoplasma, Rubella,
CMV, HSV
2. HIV , varicella , enteroviruses and
Syphilis
Routes
Transplacental – toxoplasmosis, most viruses
Ascending cervical infections – bacteria
During birth – HSV II
Can result in
Developmental malformations
Encephaloclastic lesions (brain destruction)

4. Imaging modalities
• CT- plain and contrast
• MRI- T1 , T2 axial saggital and coronal ,T2/
FLAIR- for vasogenic edema
DWI/ADC- For restriction and T2 GRE
and SWIfor
haemorrhage and calcification

5. CM
V
• Most common congenital CNS infection (DNA; Herpes virus)
• Can also cause SNHL, cardiac anomalies, hepatosplenomegaly
• Predilection for periventricular subependymal germinal matrix
• Widespread periventricular tissue necrosis and subsequent
dystrophic calcification.
• Other sites- cerebral white matter, cortex, cerebellum and
brainstem

6. •Imaging
• US/CT/MRI –
encephaloclastic lesions,
periventricular ca++,
subependymal
paraventicular cyst,
ventriculomegaly
• MRI- delayed myelination,
encephalomalacia,
migrational disorder
(lissencephaly,
polymicrogyria, pachygyria)

9. TOXOPLASMO
SIS
•T. gondii, obligate intracellular parasite
•Multifocal, scattered lesions (basal ganglia, cortical
and subcortical region, periventricular location )
•Macrocephaly **with hydrocephalus and
ependymitis.
•No migrational disorder**
Triad (imaging)
• hydrocephalus (due to ependymitis-leads to
periaqueductal necrosis-aqueductal stenosis)
• b/l chorioretinitis

11. Axial unenhanced CT
image reveals a
peripherally calcified
lesion (arrow) in the
right caudate head that
is a sequela of previous
toxoplasmosis infection.
The low-attenuation
mass lesion with
surrounding edema
in the region of the left
basal ganglia is from a
new focus of
toxoplasmosis.

12. RUBEL
LA
•Inhibits proliferation of
immature
undifferentiated progenitor
cells in germinal matrix.
•Before 12 wks- fetal
demise, stillbirth/severe
birth defect
•Congenital rubella syndrome-
1st trimester infection
•CNS – microcephaly, cortical
/basal ganglia calcification
•Others
• Cataracts,
glaucoma,
chorioretinitis
•Cardiac anomalies
•Deafness

13. Axial NECTin congenital Rubella infection showingextensive
calcifications in basal ganglia, cerebralwhite matter andcortex

14. Congenital Herpessimplex
• HSV -2
• Findings 2-4 wks after birth
• Diffuse brain involvement
• CT
-focal/diffuse white matter
lucency, relative
hyperdense cortex
- hemorrhagic infarcts/ thrombosis
-diffuse atrophy &
multicystic
encephalomalacia
later
MRI
- diffuse white matter edema,
hemorrhagic infarcts/thrombosis,

15. Zikavirus infections
•Pathology :Fetal germinal
matrix Imaging CT :
1.cerebral calcification(GM-WMis most common
site)
2. cerebral, cerebellar and brainstem volume loss
3. ventriculomegaly and microcephaly
4. polymicrogyria, lissencephaly and pachygyria
5. occipital and periventricular cysts
MRI( SWI ) : depict parenchymal Calcifications
Cortical migration defect
ventriculomegaly

17. Perinatal (congenital)HIV
•Perinatal transmission –m.c. route
•Only 1/3rd of infected mother can transmit.
•CNS symptoms – HIV encephalitis
•NECT –Diffuse cerebral atrophy (nearly 90%
cases)
- Basal ganglia calcifications (1/3rd
cases)
- Hemorrhage (thrombocytopenia)

19. Meningitis
Infective or inflamatory process of dura
mater, leptomeninges (pia and arachnoid)
and CSF within subarachnoid space.
Pachymeningitis (dura + arachnoid)
Meningoencephalitis (+ underlying
parenchymal inflamation)
Types of meningitis:
• Acute pyogenic meningitis
• Acute lymphocytic meningitis(Viral)
• Chronicmeningitis (any infectious agent including fungi and
parasites)

20. Role of CT in
meningitis
• to identify contraindications of a lumbar puncture
• to identify complications .
• CT scans may reveal the cause of meningeal
infection.
• Otorhinologic structures and congenital and
posttraumatic
calvarial defects can also be evaluated
• CT cisternography may depict CSF leaks, which may
be the source of infection in cases of recurrent
meningitis

21. Nonenhanced CT scan
findings
• may be normal (>50% of patients)
• effacement of basilar & convexity cisterns by
inflammatory exudates and brain swelling
• may demonstrate mild ventricular dilatation and
effacement of sulci
• cerebral edema and focal low-attenuating lesions.
• Sequelae from meningitis like periventricular and
meningeal
calcifications

22. Contrast-enhanced CT
scans
•Meningeal & ependymal enhancement
•Help in detecting complications of meningitis,
such as
• subdural empyema
• Venous thrombosis, infarction
• Cerebritis/abscess
• Ventriculitis.

25. •Role of neuroimaging
studies : typically used to monitor
complications.
•Complications
•Hydrocephalus
•Ventriculitis/ependimitis
•Subdural effusion/empyema
•Cerebritis/abscess
•Infarcts
(vasculitis/vasospasm)
•Dural sinus
thrombosis/venous infarcts
•Cerebral edema

27. Acute lymphocytic meningitis(viral)
• Benign & self limited
• Viral in origin
• Enterovirus (50-80%) –
echovirus, coxakie viurs and non
paralytic polio virus, mumps,
EBV, arbovirus
• Imaging usually normal unless
coexisting encephalitis
• Brain swelling and

28. Chronicmeningitis
• Tubercular(most common),
coccidiodomycosis, cryptococcus
• Hematogenous spread from the pulmonary
tuberculosis is the common mechanism.
• Predominantly basilar exudates
• Sequelae- Pachymeningitis, ischemia/infarcts,
atrophy, calcifications.

29. Imaging
• NECT- shows “en plaque” dural
thickening and
popcorn like calcifications particularly
around basal cisterns.
- meningeal enhancement
- atrophy, infarction
• MR
I
-contrast enhanced T1W Image
shows
characteristic basal
meningeal enhancement

31. Pyogenicparenchymalinfections
• Cerebritis/cerebral abscess
• Complications of cerebral
abscess

32. Cerebritis/cerebralabscess
• Focal cerebritis( focal usually pyogenic infection
without capsule or pus formation) is the earliest
stage of pyogenic brain infection from which the
abscess evolves.
Sources-
1. Directextension from adjacent structures (in about
half of cases)
2. Haematogenous
3. Penetrating trauma

33. Early cerebritis(3-5days)-
• Initial phase of abscess.
• Focalinfection
• Uncapsulated mass of congested vessels
with perivascular PMNs infiltration and
edema develops.
Late cerebritis(7-10 days)-
• central necrotic core forms ,surrounded by
outer ill- defined ring of inflammatory cells,
macrophage, granulation tissue and fibroblast.
Pathological
stages

34. Early Capsule(10-14 days)-central core of liquified
necrotic debris surrounded by well delineated capsule
composed of collagen and reticulin, initially thin and
incomplete ,more collagen deposited, becomes thicker.
Gliosis begins at periphery.
Late Capsule(>14 days)-capsule is complete & has 3 layers-
1.inner inflammatory layer of macrophage and granulation
tissue 2.middle collagenous layer
3.Outer gliotic layer
• Late capsule stage lasts for several weeks to months.
• Cavity gradually shrinks and abscess heals.

35. • Early cerebritis- normal or may show poorly marginated
subcortical hypodense area with ill-defined enhancement
in CT.
MRI- poorly marginated subcortical hyperintense area in T2WI.
- ill-defined contrast enhanced area within hypointense edema
onT1 Images.

36. Late cerebritis- central low density with
irregular enhancing rim, surrounding
vasogenic edema

37. • Early capsule- Thin(<5mm),well-delineated, distinct capsule that
enhances strongly, uniformly and continuosly, surrounding edema
present, thinner medial/ventricular margin. Rim is iso-
hyperintense on T1 & iso- hypointense on T2WI

39. • Latecapsule- sizeof abscessgradually shrinks, edema diminishes. Rim
enhancement persists for months. Hypointense rim in T2images
late capsule stage abscess: (Left) Axial T2WI MR shows a hyperintense mass with a
hypointense rim at the gray-white junction , surrounding vasogenic edema.
(Right) Axial T1 C+ MR shows a thick wall of enhancement

40. Ringenhancing lesionsD/D
D/D Features
Metastasis GW junction; multiple
Abscess Restriction of diffusion in DWI d/t high viscocity of central
necrosis Smooth hypointense rim in T2WI
Glioma (GBM) Thick irregular wall
Elevated perfusion inhigh grade glioma in perfusion MRI
Infarct (subacute) Usually gyral enh;
Costusion (subacute to chronic)
Demyelination (MS) the ring is incomplete and open towards the cortex
Radiation necrosis Low perfusion in perfusion MRI
Others Toxoplasmosis; Primary CNS lymphoma in AIDS

41. Encephalitis
• Diffuse, nonfocal brain parenchymal inflammatory
disease due to spectrum of agents
• Viral
• Non viral
• Auto immune encephalitides –
ADEM(post infective/vaccination)

42. Herpessimplexencephalitis
• Most common viral encephalitis
• HSV 1usually activation of latent infection in
trigeminal ganglion
• Fulminant, necrotising, hemorrhagic; considerable
mass effect.
• Mortality upto 55%.
• Predilection for limbic system- inferomedial temporal
lobe, orbital surface of frontal lobe , insular cortex,
cingulate gyrus

43. •Imaging
• CT – often normal in
early disease.
• In adults, CT classically
reveals hypodensity in
the temporal lobes with or
without frontal lobe
involvement, usually with
mass effect. Hemorrhage
appear slightly later.
• CECT – ill defined patchy or
gyriform enhancement
• In chronic stage – large
low density areas with
associated local atrophy
in the affected region.

45. Togavirus(JapaneseEncephalitis)
Deep-seated structures characteristically involved:
subcortical white matter (top arrow), thalami (middle
arrow), and substantia nigra (bottom arrow)

46. Acute disseminated encephalomyelitis(ADEM)
• Monophasic demyelinating disorder that occur after
vaccination or viral illness.
• Fulminant course, results in encephalopathy and focal
neurological deficits, and usually resolve without long term
sequelae.
• MRI – multiple large irregular T2 hyperintense lesions in
subcortical white matter, cerebellum and brain stem.

47. D/D

48. CNStuberculosis
• CT: non caseating granuloma –hyper/isodese with homogenous
enhancement, caseating granulomas enhance peripherally ,
target sign

49. • MRI:
non caseating granuloma- iso/hypointense on T1 & hyperintense
on T2 with homogenous C++
Caseating solid granuloma- hypointense on T1 & strikingly
hypointense on T2
Granulomas with central liquefaction- hypo on T1 & on T2 hyper
with peripheral hypointense rim

53. Parasiticinfections
• NCC
• Echinococc
osis
• Amebiasis
• Paragonimias
is
• Spargonimias
is
• Malaria

54. Neurocysticercosis
• Larval form of T. solium – cysticercus cellulosae
• Most common CNS parasite
• location
• Subarachnoid space
• Brain parenchyma- corticomedullary junction
• Intraventricular in 20-50% cases
• Dying larva incite host inflamatory reaction & calcifies
later

55. Pathological stagesandImaging
• Vesicular: Cyst with “dot” (scolex), no edema, no
enhancement. (MRI - cyst is isointense to CSF and scolex
is isointense to white matter)
• Colloidal vesicular: Ring enhancement, edema
striking Cyst contents hyperintense on T1- and T2-
weighted images (proteinaceous fluid), cyst wall is
thick and hypointense)
• Granular nodular: Faint rim enhancement, edema
decreased
• Nodular calcified: CT Ca++, MR “black dots”

58. D/D
• Subarachnoid NCC: TB meningitis (thick basilar
exudate)
• Parenchymal NCC: Abscess ( restricts strongly in
DWI)
• Intraventricular
NCC : colloid
cyst(solid)
Ependymal cyst(cystic but not
scolex) Choroid plexus cyst

59. Echinococcosis
•Larval stage- hydatid cyst
•Cerebral hydatid- seen in only 2% cases
•Imaging
• Single thin walled spherical CSF density cyst
• Large cystic lesion lying subcortically in middle
cerebral territory of parietal area (can reach large size
often over 6 cm in diameter).
• No edema or enhancement or adjacent calcification.
• Enhancement and perilesional edema are seen only if the
cyst is superinfected.

62. Prion infection Creutzfeldt–
Jakob disease(CJD)
• The typical MRI appearance of
CJD is cortical ribboning,
which describes ribbonlike
FLAIR hyperintensity and
restricted diffusion of the
cerebral cortex. The basal
ganglia and thalami are also
involved. There is often sparing
of the motor cortex.
• The pulvinar sign describes
bright DWI and FLAIR signal
within the pulvinar nucleus of
the thalamus. The hockey
stick sign describes bright
DWI and FLAIR signal within
the dorsomedial thalamus and
pulvinar.

65. COVID-19
• COVID-19–associated acute necrotizing hemorrhagic
encephalopathy, a rare encephalopathy that has been associated
with other viral infections but has yet to be demonstrated as a result of
COVID-19 infection.
• Acute necrotizing encephalopathy (ANE) is a rare complication of
influenza and other viral infections and has been related to intracranial
cytokine storms, which result in blood-brainbarrier breakdown, but
without direct viral invasion or parainfectious demyelination. Severe
COVID-19 might have a cytokine storm syndrome
• Cortical signal abnormalities, particular attention was paid to
presence of subtle hemorrhagic changes or leptomeningeal
enhancement. Additionally, acute cerebrovascular disease, venous
thrombosis, and chronic parenchymal changes were also seen in

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