Imaging evaluation of spectrum of infective pathologies of CNS including encephalitis,meningitis,abscesses,congenital pathologies and hiv associated conditions etc.

1. CNS INFECTIONS
BY - DR. SAHIL CHAUDHRY
MODERATOR - DR.PRAVEEN JOHN
AJIMS MANGALORE

2. CLASSIFICATION
• Congenital/Neonatal
Infections of the Brain
– Cytomegalovirus
– HIV Infection
– Herpes Simplex
– Toxoplasmosis
– Rubella
• Meningitis
• Pyogenic Parenchymal
Infections
– Cerebritis & Abscess
• Encephalitis
– Herpes Simplex Encephalitis
– Japanese Encephalitis
– HIV Encephalitis
• Tuberculosis
• Fungal Infections
• Parasitic Infections
– Neurocysticercosis

3. Congenital CNS Infections
• Congenital infections are typically caused by the so-
called TORCH agents:
– TOxoplasmosis
– Rubella
– Cytomegalovirus
– Herpes Simplex Virus
• Other important agents are Human Immunodeficiency
Virus & Syphilis
• These infections have severe effects on the developing
brain and can result in Developmental Brain Anomalies

4. Cytomegalovirus Infection
• Congenital infection caused by transplacental transmission of human
herpes virus
• Best diagnostic clue
– Microcephaly (Prior to 18 wks )
– Cerebral calcification (40-70%)
• Periventricular (sub ependymal)
– Cortical gyral abnormalities like Agyria ~ pachygyria ~ diffuse polymicrogyria
~ focal cortical dysplasia (18-24 wks )
– Cerebellar hypoplasia
– Myelin delay or destruction (Third trimester )
• Location:
– Dystrophic periventricular Ca++ has predilection for germinal matrix zones
• Gestational age at time of infection determines pattern of CNS injury

5. Cytomegalovirus Infection - NECT
• 4-month-old patient with congenital CMV infection show multiple foci of dystrophic
intraparenchymal calcifications, especially in the periventricular distribution.
• Cortical abnormalities are also seen in the right frontal cortex (arrows).
• Ventricular dilatation and WM volume loss.

6. Cytomegalovirus Infection - NSG Findings
• Periventricular echogenicity and
focal calcification
• Ring-like regions of periventricular
lucency may precede Ca++
• Periventricular pseudocysts and
ventricular adhesions
• Cerebellar hypoplasia

7. Cytomegalovirus Infection - MRI
• TIWI
– Periventricular subependymal foci of Tl shortening due
to Ca ++
– Ventricular dilatation and periventricular WM volume
loss
– Cerebellar hypoplasia
• T2WI
– Cortical gyral abnormalities - Ranging from agyria to
focal cortical dysplasia
– Myelination delay or destruction
– Periventricular pseudocysts
– Focal WM lesions with increased T2 (gliosis)
predominately in parietal deep WM
– Late T2 signal changes affect white matter between
juxta-cortical and periventricular layers

8. • FLAIR:
– Focal,patchy, or confluent regions of increased signal
due to gliosis
• T2* GRE:
– Periventricular decreased signal due to Ca++
• MRS:
– Decreased NAA/Cr ratio due to loss of neuronal
elements, Increased myoinositol (gliosis)

9. Cytomegalovirus Infection

10. Congenital HIV Infection
• Best diagnostic clue: Basal ganglia Ca++, volume loss
• NECT
– Atrophy (57-86%), frontal> BG > diffuse
– BG Ca++ (30-85%) > frontal white matter (WM) > cerebellum
• CECT:
– May show faint enhancement of BG prior to appearance of
Ca++

11. Congenital HIV Infection - MRI
• T1WI:
– Atrophy
• T2WI:
– High signal in frontal subcortical WM if progressive
encephalopathy
• T2* GRE:
– May accentuate Ca++
• T1 C+:
– Faint BG enhancement initially
• MRA:
– Fusiform vasculopathy (late)
• MRS:
– Decreased NAA, Increased Cho/Cr, presence of amino
acids

12. Congenital HIV Infection - MRI
• Axial (FLAIR) imaging (A, B) in a 4-year-old child infected with in
utero HIV shows marked brain parenchymal volume loss with ill-
defined areas of FLAIR hyperintensities in the white matter of
bilateral cerebral hemispheres (arrows).

13. Coronal oblique catheter angiogram shows
fusiform dilation of the ICA, proximal MCA
consistent with HIV vasculopathy
Axial NECT shows bilateral and symmetrical
calcificadons in the basal ganglia, mostly in the
globi pallidi

14. Congenital HIV Infection – D/D
• Cytomegalovirus
– Periventricular Ca++
• Microcephaly
– Neuronal migration anomalies,
cortical dysplasias
– Congenital toxoplasmosis
– Scattered Ca++
– Hydrocephalus

15. Congenital Herpes Simplex Virus Infection
• Best diagnostic clue: Ca++ in GM, hypodensities in
WM, cysts, cortical enhancement
• NECT
– Severe atrophy
– Ca++ in basal ganglia (BG), thalami, cortex, subcortical
WM
• Occasional bleeds - same locations
– Hydrocephalus, cysts
• CECT:
– Enhancement of cortex

16. • T1WI
– Atrophy, low signal in WM, cysts, hydrocephalus, bleeds
– Dysplastic cortex
• T2WI
– High signal in WM - cyst formation
– Cerebellar high signal in 50% of patients
• Tl C+
– Patchy enhancement - in cortex
– Meningeal enhancement
• MRS
– May show increased Cho during acute period, Decreased
NAA
– Chronic stage - all metabolites low

17. • Neonatal HSV 2. (A, B)
– Axial CT head images in a newborn
with seizures show multifocal
areas of hypoattenuation in the
cerebral hemispheres, especially
in left frontal and bilateral parietal
lobes.
• (C) Axial T2-weighted and (D)
diffusion-weighted images show
– Multifocal areas of T2
hyperintensity and restricted
diffusion in both cerebral
hemispheres and involving both
the cortex and underlying white
matter.
• This patient had HSV 2 virus on
cerebrospinal fluid examination.

19. Congenital Toxoplasmosis
• Caused by Toxoplasma gondii, an intracellular parasite that infects
birds and mammals.
• Human infection occurs through consumption of undercooked,
infected meat or by ingestion of infectious oocysts.
• Parasites are disseminated hematogenously to the placenta and
the fetus.
• Tansmission rate from the mother to the fetus increases with each
trimester, the severity of infection decreases with each trimester.
• Within the cranium there is diffuse inflammation of the meninges,
with varying sized granulomatous lesions.

20. • Inflammation of the ependyma (ependymitis)
causes obstruction of the cerebral aqueduct
leading to hydrocephalus.
• Unlike CMV infection, there is no malformation of
cortical development seen with toxoplasmosis
• Clinically significant abnormalities occur when
the fetus is infected before 26 weeks of
gestational age.

21. Congenital Toxoplasmosis
• Multiple discrete
intraparenchymal
and periventricular
calcifications.
• Calcifications are
seen in the basal
nuclei,
periventricular
regions, or cerebral
parenchyma.

22. Congenital Toxoplasmosis
• 11-week-old patient with
congenital toxoplasmosis show
massive hydrocephalus caused by
aqueductal stenosis.
• There are calcifications in bilateral
basal nuclei (arrows) and
calcification of the ependyma
(arrowhead).
• In infants with severe infection,
there is marked destruction with
hydrocephalus, porencephaly, and
extensive basal ganglia
calcifications.
• In cases with mild infection
(typically after the 30th week of
gestation) there is mild ventricular
enlargement and few intracranial
calcifications.

23. Congenital Rubella
• Axial T2-weighted MR imaging (A, B) in a 2-year-old patient with congenital
rubella infection shows multifocal areas of T2 hyperintensities in the white
matter of bilateral cerebral hemispheres (arrows) with delayed brain myelination
patterns are also seen
• On imaging, there can be intracranial calcification in basal ganglia,
periventricular region & cortex.

24. MENINGITIS

25. Meningitis
• Inflammatory infiltration of the pia mater, arachnoid, and CSF
• Commonly related to hematogenous dissemination from a
distant infection
• Can be divided into acute pyogenic (bacterial), lymphocytic
(viral), & Chronic (TB) Meningitis.
• Best diagnostic clue:
– Positive CSF by lumbar puncture
Morphology
– Smooth, intense leptomeningeal enhancement typical
– TB, fungal meningitis are often basilar and confluent; may be
nodular
• • Imaging may be normal early.

26. Meningitis
• NECT
– Normal study is most common
– Mild ventricular enlargement
– Subarachnoid space enlargement
– Basal cisterns effaced
• CECT
– Enhancing exudate in sulci, cisterns may be seen
– Low density areas related to perfusion alterations
• CTA: Arterial narrowing, occlusion

27. Meningitis
• Tl WI:
– Exudate is isointense
• T2WI:
– Exudate is hyperintense
• FLAIR:
– Hyperintense signal in sulci, cisterns
• Tl C+:
– Exudate typically enhances
• MRA:
– Arterial narrowing, occlusion

28. A, Gyriform hyperintensities are seen bilaterally and along the
interhemispheric fissure on this T2-weighted image.
B, Gadolinium-enhanced MRI study shows enhancement along the
cerebral sulci bilaterally.

29. Meningitis
• (A) Axial FLAIR image through the brain shows increased signal along
the left parietal cerebral sulci (arrowheads) in a patient with
meningoencephalitis.
• (B) Corresponding axial T1WI shows localized pial enhancement
along the parietal sulci and overlying meninges (arrowheads).

30. Pachymeningitis in a patient with bacterial meningitis , T1+C shows also
subdural empyemas on the left side

31. Subdural empyema with strand in a patient with bacterial meningitis , CT+C shows a
bilateral subdural effusion with cortical surface enhancement (empyema) , note
that the attenuation of the effusion is higher than that of the cerebrospinal fluid

32. Pyogenic
Parenchymal
Infections

33. Cerebral Abscess
• Focal pyogenic infection of the brain parenchyma, typically
bacterial; fungal or parasitic less common
• Four pathologic stages:
• Early cerebritis,
• late cerebritis,
• early capsule,
• late capsule

34. • Best diagnostic clue
– Imaging varies with stage of abscess development
– Early capsule: Well-defined, thin-walled with enhancing rim
– Ring-enhancing lesion with High signal (restricted diffusion) can
be seen on DWI, low ADC
– T2 hypointense abscess rim with surrounding edema
• Location
– Typically supratentorial, but may occur infratentorial (up to
14%)
– Frontal and parietal lobes most common, gray-white junction
(hematogenous)

35. Cerebral Abscess - CT
• NECT
– Early cerebritis: Ill-defined hypodense subcortical
lesion with mass effect; may be normal early
– Late cerebritis: Central low density area; peripheral
edema, increase in mass effect
– Early capsule: Hypodense mass with moderate
vasogenic edema and mass effect
– Late capsule: Edema, and mass effect may diminish

36. • CECT
– Early cerebritis: +/- Mild patchy enhancement
– Late cerebritis: Irregular peripheral rim
enhancement
– Early capsule: Low density center with thin, distinct
enhancing capsule
• Deep part of capsule is thinnest; thickest near cortex
– Late capsule: Cavity shrinkage, thickened capsule
• May be multiloculated and have "daughter“ abscesses

37. Cerebral Abscess - MRI
• T1WI
– Early cerebritis: Poorly marginated, mixed
hypointense/isointense mass
– Late cerebritis: Hypointense center, isointense/mildly
hyperintense rim
– Early capsule: Shows Rim which is isointense to
hyperintense to WM; center hyperintense to CSF
– Late capsule: Cavity shrinks, capsule thickens
• T2WI
– Early cerebritis: Ill-defined hyperintense mass
– Late cerebritis: Hyperintense center, hypointense rim;
hyperintense edema
– Early capsule: Hypointense rim
• Related to collagen, hemorrhage, or paramagnetic free radicals
– Late capsule: Edema and diminution of mass effect

38. • DWI
– Increased signal intensity in cerebritis and abscess
– ADC map: Markedly decreased signal centrally within
abscess
• Tl C+
– Early cerebritis: Patchy enhancement
– Late cerebritis: Intense but irregular rim enhancement
– Early capsule: Well-defined, thin-walled enhancing rim
– Late capsule: Cavity collapses, thickened enhancement
of capsule
• Capsule is thinnest on the ventricular side

39. MRS:
Central necrotic area may show presence of acetate, lactate,
alanine, succinate, pyruvate, and amino acids
Resolving abscess:
Hyperintense on T2WI, FLAIR; hypointense rim when it
resolves
Small ring/punctate enhancing focus may persist for months

40. Cerebral Abscess
• Progression from cerebritis to abscess. (A, B) Axial diffusion-weighted
sequence and T1 postcontrast image demonstrate areas of restricted
diffusion in the left temporal lobe and the posterior right cerebral
hemisphere that demonstrate some poorly defined enhancement.
• (C) Follow-up axial T1 postcontrast sequence 7 days later demonstrates
progression to rim enhancement typical of abscess formation.

41. Cerebral Abscess

42. ENCEPHALITIS

43. Herpes Simplex Encephalitis (HSE)
• Typically reactivation in immunocompetent
patients
• Best diagnostic clue
– Abnormal signal and enhancement of medial
temporal and inferior frontal lobes
– Involvement of cingulate gyrus and contralateral
temporal lobe highly suggestive
• Atypical patterns seen in infants, children
– May affect cerebral hemispheres primarily

44. Herpes Simplex Encephalitis (HSE)
• NECT
– CT often normal early
– Low attenuation, mild mass effect in medial temporal lobes,
insula
– Hemorrhage is typically a late feature
– Predilection for limbic system
– Basal ganglia is spared
– Earliest CT findings is usually at 3 days after symptom onset
• CECT:
– Patchy or gyriform enhancement of temporal lobes, a late
feature

45. Herpes Simplex Encephalitis (HSE)
• TlWI
– Decreased signal in gray and white matter due to loss of
gray-white junction, mass effect
– May see subacute hemorrhage as increased signal
within edematous brain
– Atrophy and encephalomalacia, in chronic cases
• T2WI, PD/Intermediate & FLAIR :
– Increased signal in gray, subcortical white matter
– Typically bilateral, but asymmetric
• T2* GRE:
– If hemorrhagic, hypointensity "blooms“ within
edematous brain

46. • DWI:
– May be hyperintense (restricted diffusion)
• Tl C+
– May see mild, patchy enhancement early
– Gyriform enhancement usually seen 1 week after initial
symptoms
– Meningeal enhancement is occasionally seen
– Enhancement is seen in temporal lobes, insular cortex,
subfrontal area and cingulate gyrus
• MR findings may be seen within 2 days of symptoms

47. Herpes Simplex Encephalitis (HSE)

48. DDX- ACUTE INFARCT,GIOLAMATOSIS CEREBRI,HHV 6 ,LIMBIC
ENCEPHALITIS

49. • VZV-MENINGITS WITH CEREBELLITIS
• EBV-BG THALAMI BRAIN STEM SPLENIUM
• WEST NILE VIRUS-SIMILAR TO EBV
• SSPE-ATROPHY WITH INV. CORTEX ,SCWM,BG
•

50. Japanese Encephalitis
• Japanese encephalitis (JE) is a flaviviral encephalitis that is a
major health problem in Asia, where it is a leading cause of
viral encephalitis with 30,000 to 50,000 cases reported
annually.
• Case fatality rates are reported as up to 60%.
• Lesions are typically T2 hyperintense and T1 hypointense
on MR imaging, and are seen involving the thalami and
brainstem, in particular the substantia nigra, basal ganglia,
cerebral cortex, corpus striatum, and cerebellum.
• The most consistent finding in JE is bilateral thalamic
lesions with or without hemorrhagic changes on MR
imaging.

51. Japanese Encephalitis
• (A, B) T2-weighted image demonstrates abnormal signal
involving the midbrain (A) and bilateral thalami (B).

52. ENCEPHALITIS LETHARGICA

53. BICKERSTAFF ENCEPHALITIS
VZV
CMV

54. RASMUSSEN ENCEPHALITIS

55. Tuberculosis
• Typically causes tuberculous meningitis (TBM)
and/or localized CNS infection, tuberculoma
• Best diagnostic clue
– Basilar meningitis + extracerebral TB (pulmonary)
– Meningitis + parenchymal lesions is highly suggestive
• Location
– TBM: Basal meningitis
– Tuberculomas: Typically parenchymal, supratentorial
(often parietal lobes)
• Infratentoriallesions are less common, can involve brainstem
(up to 8%)
• Dural tuberculomas may occur

56. Tuberculosis - CT
• NECT
– TBM: May be normal early (10-15%)
• Isodense to hyperdense exudate effaces CSF spaces, fills
basal cisterns, sulci
– Tuberculoma
• Hypodense to hyperdense round or lobulated nodule/mass
with moderate to marked edema
• Ca++ uncommon (approximately 20%)
• CECT
– TBM: Intense basilar meningeal enhancement
– Tuberculoma: Solid or ring-enhancing
• "Target sign": Central Ca++ or enhancement surrounded by
enhancing rim (not pathognomonic for TB)

57. Tuberculosis - MRI
• T1WI
– TBM: Exudate isointense or hyperintense to CSF
– Tuberculoma
• Noncaseating granuloma: Appear Hypointense to brain
• Caseating granuloma with solid center: Appear Hypointense
or isointense to brain
• Caseating granuloma with necrotic center: Appear
Hypointense or isointense to brain with central hypointensity
• Caseating granulomas may have hyperintense rim
(paramagnetic material)

58. • T2WI
– TBM: Exudate appears isointense or hyperintense to
CSF; may see low signal nodules (rare)
– Tuberculoma
• Noncaseating granuloma: Hyperintense to brain
• Caseating granuloma with solid center: Iso- to hypointense
with hypointense rim (hypointensity due to free radicals, solid
caseation or increased cellular density)
• Caseating granuloma with necrotic center: Has Central
hyperintensity with hypointense rim
• Hypointense rim + surrounding edema common

59. • TI C+
– TBM: Marked meningeal enhancement, basilar
prominence; may be nodular
• Punctate/linear basal ganglia enhancement = vasculitis
– Tuberculomas
• Noncaseating granuloma: Nodular, with homogeneous
enhancement
• Caseating granuloma with solid center: Have Peripheral
rim enhancement
• Caseating granuloma with necrotic center: Peripheral
rim-enhancement, central low signal

60. Tuberculosis - MRI
• FLAIR
– TBM: Increased intensity in basal cisterns, sulci related to
proteinaceous exudate
– Tuberculoma: Similar to T2 characteristics
• DWI
– May show hyperintense center of tuberculoma
• MRS
– TB abscess has prominent lipid, lactate but no amino acid
resonances

61. CT+C in a patient with tuberculous meningitis demonstrating marked
enhancement in the basal cistern and meninges with dilatation of the
ventricles

62. CT+C of a child with tuberculous meningitis demonstrating acute hydrocephalus and
meningeal enhancement

63. CT+C reveals avid enhancement in the basilar cisterns

64. T1+C shows basal exudates and hydrocephalous

65. TB meningitis with tuberculoma

66. Extensive infarcts of the right basal ganglia and internal capsule after the
appearance of vasculitis in the thalamoperforating arteries in a child
treated for tuberculous meningitis

67. T2 of a biopsy-proven right parietal tuberculoma , note the low signal
intensity rim of the lesion and the surrounding hyperintense vasogenic
edema

68. T1+C in a child with a tuberculous abscess in the left parietal
region , note the enhancing thick-walled abscess

69. Multiple enhancing tuberculomas in both cerebellar
hemispheres

70. Multiple ring enhancing tuberculomas

71. Fungal Diseases
• Blastomycosis: Rare, sporadic, caused by B dermatitidis,
generally affecting lungs/skin
• Coccidioidomycosis: Sporadic, relatively common, caused by C
Immitis, generally affecting lungs
• Histoplasmosis: Common, due to inhalation of H Capsulatum
(found in animal/bird feces)
• Candidiasis: Relatively common, opportunistic affects
immunosuppressed patients
• Best diagnostic clue:
– Meningeal enhancement, multiple enhancing non-specific
appearing lesions in brain and/or spinal cord in immunosuppressed
patient
• Location:
– Meninges, brain, spinal cord, vertebral bodies + discs

72. Fungal Diseases - CT
• NECT
– Areas of low density ~ lacunar infarctions (infarcts
may be larger)
– Diffuse brain edema, herniations, Hemorrhages
– Hydrocephalus
– Vertebral body destruction
• CECT
– Multiple foci of non-specific enhancement
– Some are ring-like

73. Fungal Diseases - MRI
• T1WI:
– Ill-defined areas of decreased signal intensity
• T2WI , PD/Intermediate & FLAIR:
– Focal or diffuse areas of increased signal
– Spine: Increased Signal in vertebrae, disc and spinal cord
• T2* GRE:
– May accentuate Ca++ or presence of blood products
• DWI:
– Slightly bright on trace images but no restricted diffusion
on ADC map

74. Fungal Diseases - MRI
• Tl C+
– Meningeal enhancement
• Thick meningeal enhancement  thick acute exudates or
meningeal fibrosis
– Areas of non-specific appearing enhancement, may be
ring-like, solitary-to-miliary
• May be seen in spinal cord
– Enhancement of disc, vertebrae and epidural space 
discitis/osteomyelitis
• MRA:
– Vessel irregularities (vasculitis), occlusions, mycotic
aneurysms
• MRS:
– Mildly increased Cho, decreased NAA, increased lactate

75. Fungal Diseases

77. BLACK TURBINATE SIGN – ASPERGILLOSIS ,RHINOCEREBRAL MUCORMYCOSIS

78. Neurocysticercosis
• Intracranial parasitic infection caused by the pork tapeworm,
Taenia solium
• Four pathologic stages: Vesicular, colloidal vesicular, granular
nodular, nodular calcified
• Best diagnostic clue:
– Cyst with "dot" inside
• Location
– Convexity subarachnoid spaces most common
– May involve cisterns> parenchyma> ventricles
– Parenchymal cysts often hemispheric, at gray-white junction
– Intraventricular cysts are often isolated
• Fourth ventricle is most common
– Basal cistern cysts may be racemose (grape-like)
– Rare CNS locations: Sella, orbit, spinal cord

79. Neurocysticercosis - CT
• NECT
– Vesicular stage (viable larva): Smooth, thin-walled
cyst, isodense to CSF, no edema
• Hyperdense "dot" within cyst = proto scolex
– Colloidal vesicular stage (degenerating larva):
Hyperdense cyst fluid with surrounding edema
– Granular nodular (healing) stage: Mild edema
– Nodular calcified (healed) stage: Small, Ca++ nodule

80. • CECT
– Vesicular stage: No (or mild) wall enhancement
– Colloidal vesicular stage: Thicker ring-enhancing
fibrous capsule
– Granular nodular stage: Involuting enhancing nodule
– Nodular calcified stage: Shrunken, calcified nodule
– Subarachnoid lesions: Multiple isodense cysts without
scolex

81. Neurocysticercosis - MRI
• T1WI & T2WI
– Vesicular stage: Cystic lesion isointense to CSF
• May see discrete, eccentric scolex
• No surrounding edema
– Colloidal vesicular stage: Cyst is mild to moderate
hyperintense to CSF
• Surrounding edema, mild to marked
– Granular nodular stage: Thickened, retracted cyst
wall; edema decreases
– Nodular calcified stage: Shrunken, Ca++ lesion

82. • FLAIR
– Vesicular stage: Cystic lesion isointense to CSF
• May see discrete, eccentric scolex (hyperintense to CSF); no
edema
– Colloidal vesicular stage: Cyst is hyperintense to CSF
• Surrounding edema, mild to marked
– Useful to detect intraventricular cysts (hyperintense)
• T2* GRE: Useful to demonstrate calcified scolex
• DWI: Cystic lesion typically isointense to CSF

83. Neurocysticercosis - MRI
• TI C+
– Vesicular stage: No enhancement typical, may see
mild enhancement
• May see discrete, eccentric scolex enhancement
– Colloidal vesicular stage: Thick cyst wall enhances
• Enhancing marginal nodule (scolex)
– Granular nodular stage: Thickened, retracted cyst
wall; may have nodular or ring-enhancement
– Nodular calcified stage: Small calcified lesion, rare
minimal enhancement

84. • In children, may see "encephalitic cysticercosis"
with multiple small enhancing lesions and diffuse
edema
• Intraventricular cysts may cause ventriculitis
and/or hydrocephalus
• Cisternal NCC may appear racemose
(multilobulated, grape-like), typically lacks scolex

85. Neurocysticercosis
• Two large left frontal
lobe cysticerci lack
identifiable scolices and
demonstrate adjacent
edema representing
colloidal vesicular stage.
Multiple smaller
cysticerci with internal
scolices and lack of
associated edema are in
the vesicular stage.
Scolices can be best seen
in these cysticerci on
postcontrast images (C
and D).

86. CT without contrast CT+C

87. CT without contrast shows calcifications

88. RACEMOSE NCC

89. Intraventricular NCC resulting in acute hydronephrosis

90. GIANT NCC WITH TRAPPED VENTRICLE

91. Lyme Disease
-Caused by the spirochete Borrelia burgdorfrei
-Can cause white matter disease with a
nonspecific imaging appearance of T2
prolongation predominantly in the subcortical
white matter
-Associated enhancement of multiple cranial
nerves or meningeal enhancement may
suggest the diagnosis

92. Sagittal (A and B) and axial (C) FLAIR show arcuate and confluent subcortical white
matter involvement and callososeptal interface involvement remarkably similar to
that in MS but without involvement of the periventricular white matter

93. Facial neuritis , a 48 year old woman with headache and peripheral right facial
palsy , prominent enhancement of seventh cranial nerve on postinfusion
axial T1 (A) and coronal spoiled gradient-recalled sequences (B)

94. T1+C (A and B) with enhancing bilateral third and fifth cranial nerves , seventh
cranial nerve

95. HYATID
T1 T2

96. LISTERIA
RHOMBENCE
-PHALITIS

97. CEREBRAL SHISTOSOMIASIS
PSEUDOTUMOUR
WITH ARBORISING
PATTERN

98. Approach To Ring Enhancing
Parenchymal Lesions

99. • Abscess :
– Typically T2 hypointense rim and DWI +
– Multiple lesions may occur related to septic emboli
• Tuberculosis:
– Tuberculomas often occur with meningitis
– Typically not cystic
• Neoplasm
– Primary or metastatic (primary often known)
– Thick, irregular margin enhancement typical
– May have cyst and mural nodule (I.e., pilocytic astrocytoma,
hemangioblastoma)

100. Arachnoid cyst
Solitary lesion with CSF density/intensity
No enhancement
Amebic encephalitis:
T1WI: Centrally hypointense mass
T2WI: Hyperintense lesions, +/- hemorrhage
May have hypointense rim
Tl C+: Heterogeneous or ring-enhancement

101. METS/EM
BOLI

102. ABSCESS

103. PILO

104. MS/TD

105. GBM

106. Mets

107. Demyelination

108. Radionecrosis

109. Enhancing subacute hemorrhagic stroke

110. CNS IMAGING IN AIDS

111. CNS disease in HIV / AIDS

112. • Up to 90% of those infected by the HIV will have CNS
involvement
• CNS infection by HIV may occur concurrently or
shortly after acute systemic HIV infection
• During this acute stage, structural neuroimaging
studies are usually normal even if the infected
individual has clinical signs of CNS involvement

113. • HIV infection of the CNS produces a progressive
cognitive-motor disorder often called the AIDS
Dementia Complex (ADC).
• As the HIV-induced brain injuries progress, cortical
atrophy and WM disease due to HIV oligodendroglial
damage occurs - HIV leukoencephalopathy. MR
and/or CT detect these changes as atrophy and white
matter disease.

114. HIV Encephalitis
• Best diagnostic clue: Combination of atrophy
and symmetric, periventricular or diffuse
white matter (WM) disease
• Location:
– Bilateral periventricular and centrum semiovale
WM, basal ganglia, cerebellum, brainstem

115. HIV Encephalitis - CT
• NECT
– Children: Atrophy and WM diffuse hypodensity
• In utero HIV infection: Characteristic bilateral and symmetrical
calcifications in basal ganglia and frontal WM with eventual
contrast-enhancement
– Adults: Normal or mild atrophy and WM hypodensity
• CECT:
– Usually no contrast-enhancement

116. HIV Encephalitis - MRI
• T1WI:
– WM abnormality may not be evident
• T2WI
– 2 imaging patterns
• Focal abnormalities of high signal intensity
• Diffuse moderate-high signal WM changes
• FLAIR
– Same imaging patterns as T2WI
– Allows early detection of small « 2 cm) lesions in
cortical/subcortical and deep WM locations

117. • Tl C+:
– No enhancement in involved regions
• MRS
– AIDS patients with CD4 < 200/mm3, neurologic
evidence of AIDS dementia complex, and atrophy
• Subcortical region shows Decrease N-acetyl aspartate
(neuronal loss) and Increased choline in WM (astrocytosis
or microglial proliferation)
– Cognitively normal and clinically asymptomatic
patients
• Subcortical region shows only increased choline

118. HIV Encephalitis

120. White Matter T2
hyperintensities
without mass effect
or enhancement.
Usually begins in the
Frontal lobes.

122. Cortical atrophy with
WM changes in
advanced HIV
encephalopathy

123. • MRS may provide means for early diagnosis and
evaluation of treatment in HIV.
NAA
Co
mI
high Cho,mI
low NAA

124. • Opportunistic infections
Toxoplasmosis
CMV, Herpes
Cryptococcosis, other fungal
PML
Mycobacteria, neurosyphilis
• Malignancies
Lymphomas
Kaposi sarcoma

125. TOXOPLASMOSIS
• MC cause of intracranial mass lesion in AIDS.
• Focal/multiple ring and /or nodular enhancing
lesions .
• Predilection for CM junctions and Basal Ganglia.
• “Asymmetric target sign”
• MRS shows decr/ absent NAA,Cho,Cr peaks and a tall
Lipid-Lactate peak.

127. TOXOPLASMOSIS

128. Progressive multifocal
leukoencephalopathy
• PML is a central demyelinating disease
resulting from the reactivation of a latent
infection of oligodendrocytes by JC
polyomavirus.
• Incidence : 4-5% of AIDS patients.
• Clinically, limb weakness is commonest
presentation, visual field defects, speech
abnormalities, ataxia and dementia may be
seen.

129. PML imaging findings
• Lesions can occur in any part of brain but are
commonest in parieto-occipital regions.
• MRI shows multifocal, asymmetric bilateral
white matter lesions that are of high signal
on T2W and low signal on T1W images.
• Extension to the subcortical U-fibres gives
the lesions a characteristic ‘scalloped’
appearance.

130. PML Imaging findings
• CT reveals asymmetric focal zones of low
attenuation that involve the periventricular
and subcortical white matter.
• This appearance is a differential diagnostic
feature compared with the typically more
symmetric areas of low attention seen in
patients with HIV encephalopathy.
• They don’t enhance and haemorrhage is
unusual.

132. PML

135. CMV
Encephalitis -
Ependymal and
subependymal
irregular T2
hyperintensities
and enhancement.

137. CRYPTOCOCCOSIS
• MC fungal infection in AIDS
• Cryptococcoma , miliary nodules,meningitis
• Symmetric perivascular spread in BG and midbrain
(Dilated Virchow Robin spaces)
+ choroid plexus granulomas, relatively specific for
cryptococcosis.

138. CNS TB

139. Herpes simplex ventriculitis

140. GELATINOUS PSEUDOCYSTS IN DILATED VR SPACES WITH SOAP BUBBLE
MORPHOLOGY

141. LYMPHOMA
• 2nd MC cause of IC mass lesion after toxoplasmosis.
• Primary CNS lymphoma- B cell NHL
• Lesions can mimic toxoplasmosis
• Predilection for BG, Thalamus, PV WM, CORPUS
CALLOSUM
• NCCT- hyper dense, periventricular with fluffy
enhancement.
• infiltrative + crossing midline

142. Imaging findings
• lower signal intensity than grey matter on T2W
MRI. This reflects the dense cellularity of
lymphoma.
• Lesions have relatively little mass effect and
oedema for their size.
• Heamorrhage is unusual and calcifications seen
only after treatment.
• Enhancement is typical in a smooth or nodular
ring surrounding a zone of central necrosis.

143. Multifocal Primary Cerebral lymphoma
BG WITH SUBEPENDYMAL SPREAD

144. Primary Cerebral lymphoma

147. Lymphoma Vs Toxoplasmosis
• Single enhancing mass lesions in AIDS is more
likely to be Lymphoma.
• Sub ependymal spread is a feature of
lymphoma.
• Thallium-201 SPECT and FDG-PET show
greater uptake in lymphoma than
toxoplasmosis.
• DWI has limited value.

148. Toxoplasma Vs Lymphoma
• MR Spectroscopy
toxoplasma
low or absent NAA, Cho, Cr
high Lipid (+Lactate)
lymphoma
low NAA, Cr
high Cho
high Lipid, lactate

149. INCREASED rCBV IN LYMPHOMA

150. DECREASED rCBV IN TOXOPLASMA GRANULOMA

151. Mild to moderate atrophy, white matter lesions, cortical and subcortical infarctions,
gummas, leptomeningeal enhancement, and arteritis have all been reported
NEUROSYPHILIS

152. Aspergillosis in an HIV-infected patient who presented with rapidly progressive
proptosis. Axial postcontrast T1-weighted imageshows a peripherally enhancing low-
signal intensity mass within the left orbit that is causing proptosis.Intracranial
extension is present,as evidenced by dural enhancement in themiddle cranial fossa
(arrow). Opacification and enhancement of the left ethmoid air cells is seen. In
addition, enhancement is seen within the periorbital soft tissue and in the left
temporalis muscle

153. Neuro Immune Reconstitution
Inflammatory Syndrome
• Two types –UNMASKING AND PARADOXICAL
• PML MCC
• NATALIZUMAB FOR MS
• RISK FACTORS –CD4 AND THERAPY INTERVAL

155. References:
• Diagnostic Neuroradiology, Osborn.
• Central Nervous System Infections, Neuroimaging
Clinics, November 2012
• Central Nervous System Infection, Neuroimaging
Clinics, November 2010
• CT & MRI of Whole Body, John Haaga.