This is nice presentation covers most of imporant intrancranial ( Brain) infection with many ct mri images . This presentation also includes cns (brain) manifestation of COVID-19 latest hot topic. This is very helpful for radiologist or radiology resident. Thanks.

1. IMAGING OF INTRACRANIAL
INFECTIONS
Pradeep Kumar

2. •Congenital / neonatal infections
•Meningitis
•Pyogenic parenchymal infections
•Encephalitis
•Tubercular and fungal infections
•Parasitic 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)
 Dystrophic calcifications

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 SWI for
haemorrhage and calcification

5. CMV
• 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. TOXOPLASMOSIS
•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
• intracranial calcifications

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. RUBELLA
•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
•CNS Imaging – similar to other
viral infections, nonspecific

13. Axial NECT in congenital Rubella infection showing extensive
calcifications in basal ganglia, cerebral white matter and cortex

14. Congenital Herpes simplex
• 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, parenchymal or
meningeal enhancement after contrast
administration

15. Zika virus infections
• Pathology :Fetal germinal matrix
Imaging CT :
1.cerebral calcification(GM-WM is 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)
• Chronic meningitis (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 meningeal
enhancement in some cases.

28. Chronic meningitis
• 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
• MRI -contrast enhanced T1W Image shows
characteristic basal meningeal
enhancement

31. Pyogenic parenchymal infections
• Cerebritis/cerebral abscess
• Complications of cerebral abscess

32. Cerebritis/cerebral abscess
• 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. Direct extension from adjacent structures (in about half
of cases)
2. Haematogenous
3. Penetrating trauma

33. Early cerebritis(3-5days)-
• Initial phase of abscess.
• Focal infection
• 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. • Late capsule- size of abscess gradually shrinks, edema diminishes. Rim
enhancement persists for months. Hypointense rim in T2 images
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. Ring enhancing lesions D/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. Herpes simplex encephalitis
• 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
• Sequential bilaterality – highly suggestive

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 (Japanese Encephalitis)
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. CNS tuberculosis
• 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. Parasitic infections
• NCC
• Echinococcosis
• Amebiasis
• Paragonimiasis
• Spargonimiasis
• 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 stages and Imaging
• 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 very few case.

68. THANK YOU