Diagnostic Imaging of Central Nervous System Infections

1. C.N.S.
CNS Infections

2. Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology
Department , Zagazig University Hospitals
Egypt
FINR (Fellowship of Interventional
Neuroradiology)-Switzerland
zaitoun82@gmail.com

5. Knowing as much as
possible about your enemy
precedes successful battle
and learning about the
disease process precedes
successful management

6. CNS Infections
1-Bacterial (Purulent) infections
2-Fungal infections
3-Parasitic infections
4-Viral infections
5-Meningitis
6-Encephalitis
7-Congenital CNS Infections
8-AIDS
9-Prion Infection

7. 1-Bacterial (Purulent) infections :
a) Bacterial Meningitis
b) Tuberculous Meningitis
c) Empyema
d) Brain Abscess
e) Lyme Disease

8. a) Bacterial Meningitis :
1-Causes
2-Pathological Types
3-Predisposing factors
4-Radiographic Features
5-Complications

9. 1-Causes :
-Neonates : Group B Streptococcus , E.coli &
Listeria
-Children : Haemophilus , E. coli & Neisseria
meningitidis
-Adults : S.pneumoniae & N. meningitidis

10. 2-Pathological Types :
a) Leptomeningitis (most common) : arachnoid
and pia involved
b) Pachymeningitis : dura and outer layer of
arachnoid involved

12. 3-Predisposing factors :
a) Sinusitis
b) Chronic pulmonary infection
c) Tetralogy of Fallot
d) Transposition of great vessels
e) Other cyanotic heart disease

13. 4-Radiographic Features :
a) Meningeal Contrast Enhancement
b) Neonatal Cranial US

14. a) Meningeal Contrast Enhancement :
-Normal CT examination is initially most common
finding
-Convexity enhancement occurring later is a typical
finding , however , lack of enhancement doesn’t
exclude meningitis
-May see generalized brain swelling &/or focal or
generalized ischemia
-Hydrocephalus

15. T1+C shows leptomeningeal enhancement (arrows)

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

17. Pachymeningitis in a patient with bacterial meningitis , T1+C shows diffuse dural
enhancement

18. T1+C shows left-sided dural enhancement (pachymeningitis) and focal pial
enhancement

19. b) Neonatal Cranial US :
-Subtle findings : abnormal parenchymal
echogenicity
-Echogenic sulci , 40 %
-Extra-axial fluid collections
-Ventricular dilatation
-Ventriculitis occurs in 70%-90% of cases of
bacterial meningitis , normally thin ventricular
wall thickens , wall becomes hyperechoic , debris
in CSF

20. 5-Complications :
a) Subdural effusion : common in infants and
children
b)Empyema
c) Parenchymal extension : abscess and
cerebritis
d) Ventriculitis
e) Hydrocephalus ( communicating >
noncommunicating)
f) Venous infarctions secondary to venous
thrombosis

21. 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

22. CT without contrast shows mild ventriculomegaly and sulcal
effacement

23. T2 shows only mild ventriculomegaly

24. Lacunar infarct in a patient with bacterial meningitis , CT shows the
distribution of the perforating vessels in the brainstem , basal ganglia &
white matter

25. Bilateral subdural empyema in a patient with bacterial meningitis , CT shows the important
diagnostic features of meningitis : prominent enhancement of the margin and increased
attenuation of the empyema

26. Abscess formation in a patient with bacterial meningitis , T1+C shows an
abscess formation in the right frontal lobe (arrows) and a right
parasagittal subdural empyema (arrowhead)

27. b) Tuberculous Meningitis :
1-Incidence
2-Radiographic Features

28. 1-Incidence :
-The most common CNS manifestation of TB followed
by intraparenchymal tuberculoma
-Seen in all age groups , although has a peak incidence
in childhood (particularly 0-4 years of age) in high
prevalence areas , in low prevalence areas it is more
frequently encountered in adolescents and adults
-Spread is usually hematogenous from pulmonary TB
-Basilar meningeal involvement by chronic
granulomatous process leads to cranial nerve palsies
(3rd
, 4th
& 6th
)

29. 2-Radiographic Features :
1-Basilar meningitis
2-Abscesses (Tuberculoma)

30. 1-Basilar meningitis :
-Indistinguishable from fungal , lymphoma and
sarcoid :
1-Intense contrast enhancement of basilar
meninges (CT & MRI)
2-T2 hypointense meninges
3-Later complications may be visible including :
a) Hydrocephalus
b) Infarcts due to arteritis (especially in children)
4-Calcifications occur late in disease

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

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

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

34. T1+C shows basal exudates and hydrocephalous

35. TB meningitis with tuberculoma

36. 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

37. 2-Abscesses (Tuberculoma) :
-Rare unless immunocompromised or from endemic
areas (Indian population)
-Usually solitary
-Nonspecific enhancing masslike lesions , not always
possible to differentiate a tuberculoma from a
pyogenic abscess
-Tends to have central hypointensity on T2 (in contrast
to a pyogenic abscess which is hyperintense) , shows
restricted diffusion
-Cerebral hemispheres and basal ganglia
-Miliary form : multiple tiny intraparenchymal lesions

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

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

40. Multiple enhancing tuberculomas in both cerebellar
hemispheres

41. Multiple ring enhancing tuberculomas

42. c) Empyema :
1-Incidence
2-Radiographic Features

43. 1-Incidence :
-An empyema is an infected fluid collection in
subdural (common , subdural effusion) or
epidural (uncommon) location
-Empyema is a neurosurgical emergency
-Cause : sinusitis (most common ) , otitis ,
trauma & post craniotomy

44. 2-Radiographic Features :
1-Subdural or epidural low attenuation fluid
collection with enhancement of adjacent brain
2-Thick curvilinear enhancement of empyema
3-Venous infarction → edema → mass effect →
midline shift
4-Diffusion imaging is highly sensitive : lesions
are DWI bright and ADC dark
5-Concomitant signs of sinusitis , otitis

45. T1+C

46. T2 T1+C

47. Diffusion

48. d) Brain Abscess :
1-Common Organism
2-Mechanism
3-Radiographic Features
4-Differential Diagnosis

49. 1-Common Organism :
-Children : Staphylococcus (especially after
trauma) , Streptococcus & pneumococcus
-Adults : Mixed aerobic and anaerobic flora
-Immunosuppression : Toxoplasmosis ,
cryptococcosis , candidiasis , aspergillosis,
nocardiosis , mucormycosis (diabetes) , TB &
atypical mycobacteria

50. 2-Mechanism :
a) Hematogenous dissemination (most
common) :
-Intravenous drug abuse
-Sepsis
b) Direct extension :
-Sinusitis
-Otitis , mastoiditis
-Complication of bacterial meningitis
-Open injury (penetrating trauma , surgery)
c) Idiopathic

51. -An abscess evolve over 4 stages :
(Early cerebritis >> late cerebritis >> early abscess >>
late abscess) and takes about 2 weeks to fully
develop , in the early stage of infection , there is
nonspecific T2 prolongation in the affected region
with heterogeneous enhancement
-After the abscess become discrete , the classic imaging
appearance is a ring enhancing lesion , the rim is
hypointe

52. 3-Radiographic Features :
a) Location
b) Morphology
c) Diffusion & Perfusion
d) MRS

53. a) Location :
1-Hematogenous seeding : multiple lesions at
GM/WM junction
2-Penetrating trauma or sinusitis : lesion around
the entry site

54. b) Morphology :
1-Early Stage of Infection
2-Thin walled ring enhancement lesion
3-Capsule formation
4-Mass Effect
5-Ventriculitis
6-Daughter Cysts

55. 1-Early Stage of Infection :
-In the early stage of infection , there is
nonspecific T2 prolongation in the affected
region with heterogeneous enhancement
2-Thin walled ring enhancement lesion :
-The classic imaging appearance

56. 3-Capsule formation in 7 to 14 days :
-Capsule is thinner on WM side because of lower
perfusion to WM than to GM , because of the
thinner capsule , daughter lesions (and
intraventricular rupture) occur on the medial side
-Capsule is hypointense on T2 , unlike the rim of a
glioma or metastases , an abscess rim is thin &
smooth
-Inner margin is often smooth
-Capsule formation may be delayed by steroid
administration

57. 4-Mass effect (abscessed cavity , edema)
5-Ventriculitis due to ventricular spread :
-Increased CSF density (elevated protein
concentration)
-Ependymal contrast enhancement
-May cause ventricular septations and
hydrocephalus
-DWI bright
6-Daughter lesions

58. c) Diffusion & Perfusion :
-High DWI signal is usually present centrally
-Often this represents true restricted
diffusion (low signal on ADC)
-rCBV is reduced in the surrounding edema c.f.
to both normal white matter and tumor
edema seen in high grade gliomas

59. d) MRS :
-Recognition of amino acids , acetate and
succinate in pyogenic abscesses and lipid peak
in tubercular abscesses

60. (a) T1+C , (b) T2 , (c) Diffusion , (d) ADC

61. T1+C

62. Diffusion

63. Diffusion

64. CT without contrast CT+C

65. CT+C

66. With Ventriculitis

67. 4-Differential Diagnosis :
1-Metastasis or high grade glioma (e.g. GBM) :
-Abscesses tend to have smoother inner wall
-Satellite lesions favour infection
-Abscesses may have low intensity capsule
-rCBV elevated in high grade gliomas , reduced in
abscesses
2-subacute infarction , hemorrhage or contusion
3-Demyelination
4-Radiation necrosis

68. GBM

69. Mets

70. Demyelination

71. Radionecrosis

72. Enhancing subacute hemorrhagic stroke

73. e) 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

74. FLAIR shows several foci of high T2 signal in periventricular white
matter on left side above the trigone of left lateral ventricle

75. FLAIR shows multiple nonspecific foci of T2 prolongation in
white matter

76. 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

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

78. T1+C (A and B) with enhancing bilateral third and fifth cranial nerves , C, Nine
days later , the patient developed left facial palsy with enhancing fundal
tuft and labyrinthine and tympanic segments of the seventh cranial nerve

79. (a) Axial T1+C shows enhancement of left seventh cranial nerve (arrow) , (b)
Coronal T1+C shows left trigeminal nerve enhancement (arrow)

80. T1+C depict enhancement of (a) right trigeminal nerve (arrow)
and (b) descending portion of the right facial nerve (arrow)

81. 2-Fungal Infections :
a) Causes
b) Radiographic Features

82. a) Causes :
1-Immunocompetent patients :
-Coccidioidomycosis , histoplasmosis &
blastomycosis
2-Immunocompromised patients (AIDS ,
chemotherapy , steroids & transplant
recipients ) :
-Nocardiosis , aspergillosis, candidiasis ,
cryptococcosis & mucormycosis

83. b) Radiographic Features :
1-Basilar Meningitis
2-Abscesses
3-Helpful Criteria

84. 1-Basilar Meningitis :
-Intense contrast enhancement of basilar
meninges (similar to TB)
2-Abscesses :
-Early : granuloma
-Late: abscess with ring enhancement and
central necrosis (A ring-enhancing T2
heterointense lesion with irregular walls and
irregular projections into the cavity with low
ADC and no contrast enhancement)

85. 3-Helpful Criteria :
a) Aspergillosis
b) Mucormycosis
c) Coccidiodomycosis
d) Cryptococcosis

86. a) Aspergillosis :
1-Hemorrhagic infarcts from vascular invasion
2-Often coexistent sinus disease that has extended to
CNS
3-Dissimenated Aspergillosis (T2W isointense /
hypointense masslike lesions)
b) Mucormycosis :
-Indistinguishable from aspergillosis
c) Coccidiodomycosis :
-Indistinguishable from TB

87. Aspergillosis in a 36-year-old woman with HIV infection who experienced a
rapid decline in consciousness , axial unenhanced CT reveals a large
parenchymal hemorrhage involving the left hemisphere that caused mass
effect and midline shift

88. Disseminated aspergillosis in a 38-year-old man with HIV infection , CT+C shows
multiple circumscribed regions of hypoattenuation with faint peripheral
enhancement

89. Disseminated aspergillosis in a 39-year-old AIDS patient , (a) T2 FLAIR shows
two well-circumscribed foci of hyperintensity within the centrum
semiovale , there is no significant surrounding edema , (b) T1+C shows low
signal intensity lesions that do not demonstrate enhancement

90. Aspergillosis in an HIV-infected patient who presented with rapidly progressive proptosis , T1+C
shows 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 the
middle 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

91. d) Cryptococcosis : Most common
1-Incidence
2-Radiographic Features

92. 1-Incidence :
-The most common CNS fungal infection in
patients with AIDS & is caused by
Cryptococcus neoformans
-It is the 3rd
most common CNS infection in AIDS
overall , after HIV encephalopathy &
Toxoplasmosis
-Similar to toxoplasmosis , AIDS patients
become susceptible to Cryptococcus with a
CD4 count less than 100 cells/µl

93. 2-Radiographic Features :
- The imaging findings may consist of
meningoencephalitis , intraventricular or
intraparenchymal cryptococcomas , gelatinous
pseudocysts or hydrocephalus
-Cryptococcus spreads along the basal ganglia
perivascular spaces leaving behind gelatinous
pseudocysts which appears as round water signal
lesions on T1 & T2
-Intraventricular or intraparenchymal cryptococcomas
(ring enhancing granulomas)
-Consider this diagnosis in an HIV-positive patient with
communicating hydrocephalus

94. T2 shows multiple foci of high signal intensity within the bilateral basal
ganglia , findings consistent with gelatinous pseudocysts in dilated
perivascular spaces (arrows) , enlargement of the ventricles , consistent
with hydrocephalus , is also present

95. Cryptococcal meningoencephalitis (a) T2 shows high signal intensity in the right
occipital lobe with foci of hyperintensity are present in the bilateral basal ganglia
(arrows) findings consistent with gelatinous pseudocysts , (b) T1 shows low signal
intensity in the right occipital lobe that corresponds to the area of hyperintensity
seen in a (c) T1+C shows leptomeningeal enhancement in the region of the T2
hyperintensity

96. Cryptococcoma (a) T1 shows a low signal intensity mass lesion in the right
cerebellum , (b) T2 shows the mass is heterogeneous in signal intensity
but predominantly hyperintense with a surrounding rim of T2
hyperintensity , a finding consistent with edema , (c) T1+C reveals
peripheral nodular enhancement of the lesion

97. 3-Parasitic Infections :
a) Neurocysticercosis
b) Toxoplasmosis
c) Hydatid Disease

98. a) Neurocysticercosis : (NCC)
1-Etiology
2-Evolution of Lesions
3-Locations
4-Radiographic Features

99. 1-Etiology :
-Most common parasitic CNS infection of
immunocompetent patients
-Caused by Taenia solium (pork tapeworm)
-Ingestion of contaminated water or pork , ingested
eggs penetrate intestine , disseminate
hematogenously and encyst in muscle , brain and
ocular tissue
-Cysts first contain a living larva which ultimately
dies causing inflammation (contrast
enhancement) and calcifications
-75% of infected patients have CNS involvement ,
seizures are the most common presentation

101. 2-Evolution of Lesions :
a) Nonenhancing cyst : live larvae
b) Ring enhancing lesion : dying larvae cause
inflammatory reaction
c) Calcification: old lesion

102. 3-Locations :
a) Parenchymal (most common)
b) Intraventricular (may cause obstruction)
c) Subarachnoid

103. 4-Radiographic Features :
a) Four Stages in Brain Parenchyma
b) Typical Appearance of Cysts
c) Other Findings

104. a) Four Stages in Brain Parenchyma :
1-Vesicular stage
2-Colloid stage
3-Nodular granular stage
4-Calcified stage

105. 1-Vesicular stage :
-Cyst + scolex , non-enhancement
2-Colloid stage :
-Ring enhancement , edema
3-Nodular granular stage :
-Decreased enhancement & edema , begins
calcification
4-Calcified stage :
-Obvious calcifications on CT & MRI (T2*W)

107. b) Typical Appearance of Cysts :
1-Multiple cystic lesions of water density
2-Larvae (scolices) appear of variable signal intensity on T2
3-Ring enhancement (inflammatory response caused by dying
larvae)
4-The cyst with dot sign :
-Represents the parasytic cyst with (usually excentric) scolex
-It can be seen on both MRI and CT at :
a) The vesicular stage (CSF like density cyst & hyperintense
scolex)
b) Colloidal vesicular stage (enhancement of wall and scolex)

108. (a) Pathognomonic subcortical cyst left showing the scolex with a close by calcification
, calcified subcortical cyst right with perifocal/perilesional edema , calcification in
the left temporal muscle , (b) ring enhancing lesion due to a degenerating
subcortical cyst in the right occipital lobe , (c) several scattered intraparenchymal
calcifications most likely in the context of NCC

109. CT without contrast CT+C

110. T1 T1+C

111. T1+C

113. CT without contrast shows calcifications

114. CT without contrast shows calcifications

115. Intraventricular NCC resulting in acute hydronephrosis

116. T1 shows extraparenchymal subarachnoid cysticercosis with multiple
lobulated cystic lesions predominantly in the subarachnoid space
(prepontine , suprasellar cistern and cisterna ambiens) as well as probable
intraventricular lesions with potential dilation of the 4th ventricle

117. c) Other Findings :
1-Hydrocephalus
2-Chronic meningitis
3-Calcification of skeletal muscle

118. b) Toxoplasmosis :
1-Incidence
2-Clinical Picture
3-Radiographic Features
4-Differential Diagnosis

119. 1-Incidence :
-2nd
most common opportunistic CNS infection in
AIDS (with CD4 count less than 100 cells/µl)
with HIV encephalitis is the most common
-Is the most common cause of cerebral
abscess in these patients
-Caused by Toxoplasma gondii (reservoir :
infected cats)

120. 2-Clinical Picture :
a) Congenital :
-Meningitis , encephalitis : calcification
-Encephalomalacia , atrophy
-Chorioretinitis

121. b) Immunocompetent adults :
-Systemic disease with lymphadenopathy and
fever
-CNS is not involved (in contradistinction to
AIDS)
c) Immunocompromised patients :
-Fulminant CNS disease
-Predilection for basal ganglia and grey-white
matter junction

122. 3-Radiographic Features :
-Solitary or multiple ring-enhancing lesions with
marked surrounding edema in basal ganglia ,
thalami and grey-white matter junction
-Target appearance of lesions is common
-Treated lesions may calcify or hemorrhage

124. NECT shows a large area of edema in the LT basal ganglia (yellow arrows) ,
centered on a subtle hyperattenuating mass (red arrow)

125. Multiple ring-enhancing lesions with surrounding vasogenic
edema

126. Ring enhancing lesion with surrounding vasogenic edema

127. T1+C shows smooth ring-enhancement of the lesion (red arrow)

128. T1+C shows multiple enhancing lesions

129. Ring enhancing lesions

130. T1+C shows ring-enhancing lesions with eccentric nodules : the
“target sign” (arrows)

131. FLAIR shows the extensive edema surrounding a heterogeneous
rounded mass (red arrow) in the LT basal ganglia

132. F-18 FDG PET scan shows asymmetrical , relatively decreased
metabolism of the LT basal ganglia (blue arrows)

133. 4-Differential Diagnosis : From Lymphoma
1-Periventricular location and subependymal
spread favors lymphoma
2-Empirical treatment with antiprotozoal drugs
followed by reassessment of lesions is often used
to distinguish between the two
3-Multiple lesions more suggestive of toxoplasma
4-SPECT thallium : lymphoma appears as hot
lesions , toxoplasmosis appears as cold lesions
5-Perfusion : Increased relative cerebral blood
volume in lymphoma
6-PET : Toxoplasmosis is hypometabolic
7-MRS : Lymphoma shows high choline peak ,
Toxoplasmosis shows high lipid peak

134. c) Hydatid Disease :
1-Incidence
2-Radiographic Features

135. 1-Incidence :
-Intracranial hydatid disease is very rare , most
of cerebral hydatid cysts are located in
supratentorial structures in the vascular
territory of middle cerebral artery
-Caused by Echinococcus granulosus

136. 2-Radiographic Features :
-Well-defined circumscribed spherical non-enhancing
intra-axial cystic lesion
-Lies in the territory of the middle cerebral artery
-Cyst fluid is isointense with CSF in all pulse sequences
-No calcification and typically no surrounding edema ,
presence of perilesional edema usually indicates
complication as rupture or secondary infection

137. CT without contrast CT+C

138. T1 T2

139. T1+C

140. DWI ADC

141. 4-Viral infections :
1-Herpes Simplex Virus Encephalitis
2-HIV Encephalopathy
3-CMV Encephalitis

142. 1-Herpes Simplex Virus Encephalitis :
a) Types
b) Clinical Picture
c) Location
d) Radiographic Features
e) Differential Diagnosis

143. a) Types :
1-HSV 2 , genital herpes :
-Neonatal TORCH infection (see Congenital
Infections)
-Acquired during delivery
-Diffuse encephalitis (non-focal)

144. 2-HSV 1 , oral herpes :
-Children and adults
-Usually activation of latent virus in trigeminal
ganglion
-Altered mental status , fulminant course
-Limbic system , frequently bilateral but
asymmetrical

145. b) Clinical Picture :
-Non specific consisting of fever , headaches ,
focal neurological deficits , seizures and
altered or decreased level of consciousness
-Diagnosis is established with PCR of CSF with
the clinical Picture , CSF demonstrating
pleocytosis and elevated protein
-Herpes should be the first consideration in any
patient with fever , mesial temporal lobe
signal abnormality and acute altered mental
status

146. c) Location :
-In the adult immunocompetent patient , the
pattern is quite characteristic involving the
medial temporal lobes & Cingulate gyrus, the
basal ganglia are typically spared , helping to
distinguish it from a MCA infarct
-In immunocompromised patients , involvement
can be more diffuse and more likely to involve
the brainstem

147. d) Radiographic Features : (of HSV-1)
1-CT
2-MRI

148. 1-CT :
-Often normal in early HSV encephalitis
-Low attenuation in within the anterior and
medial parts of the temporal lobes and the
insular cortex
-Later then the changes may become more
obvious and even progress to hemorrhage

150. 2-MRI :
*T1 :
-May show general edema (hypointense) in
affected region
-If complicated by subacute hemorrhage there may
be areas of hyperintense signal
*T2 :
-Hyperintensity of affected white matter and cortex

151. *T1+C :
-Early : enhancement is usually absent
-Later enhancement is variable in pattern :
1-Gyral enhancement
2-Leptomeningeal enhancement
3-Ring enhancement
4-Diffuse enhancement
*DWI / ADC :
-Restricted diffusion is common due to cytotoxic
edema (T1 hypointense/T2 hyperintense)

152. T2 Diffusion

153. T2 Diffusion

154. T2

155. T1 shows multifocal hemorrhages

156. e) Differential Diagnosis :
-The D.D. of medial temporal lobe lesions
include : MCA infarction , infiltrating glioma ,
limbic encephalitis and seizure related
changes
-Fever is typically absent in infarction & glioma
-Herpes encephalitis should be the first
consideration in any patient with fever &
signal abnormality in the medial temporal
lobe

157. 2-HIV Encephalopathy :
-AIDS dementia complex
-The most common CNS infection in AIDS
patients
-MRI : diffuse cerebral atrophy & symmetric T2
prolongation on the periventricular & deep
white matter , no mass effect , no
enhancement
-In contrast to PML , HIV encephalitis spares the
subcortical U-fibers & tends to be symmetric

159. (a) NECT shows prominence of the sulci and ventricles , findings consistent global
volume loss , symmetric low attenuation is present in the periventricular white
matter , (b) T2 shows prominence of the sulci and ventricles , findings consistent
with diffuse atrophy , symmetric periventricular hyperintensity corresponds to the
regions of low attenuation seen on the CT , no mass effect , (c) T1+C shows that
no enhancement is associated with the regions of T2 hyperintensity

160. T2 FLAIR

161. FLAIR

162. 3-CMV Encephalitis :
-Only affects the immunosuppressed , typically
when the CD4 cell count is less than 50 cells/µl
-The most common CNS manifestation of CMV
infection is ventriculitis or
meningoencephalitis
-The characteristic imaging feature of CMV
ventriculitis include subependymal FLAIR
hyperintensity & enhancement throughout
the ventricular system

163. (a) FLAIR shows circumferential hyperintensity surrounding the lateral and
fourth ventricles , nonspecific T2 signal is present in the white matter , (b)
T1+C reveals thin , linear periventricular enhancement , the nonspecific T2
hyperintensity in the white matter did not enhance

164. T2 FLAIR

165. 5-Meningitis :
-Diagnosis is made by lumbar puncture not
imaging
-Indications for neuroimaging in possible
meningitis are to assess complications (see
before)

166. a) Bacterial Meningitis :
-See before
b) T.B. Meningitis :
-See before
c) Subdural Effusion / Empyema :
-See before
d) Cerebritis :
-Diffuse area of parenchymal low attenuation which may
develop into abscess
e) Abscess :
-See before
f) Viral Meningitis :
-Neuroimaging usually entirely normal

167. 6-Encephalitis :
a) HSV Encephalitis :
-See before
b) Slow Viruses :
1-Subacute Sclerosing Panencephalitis (SSPE) :
-Known as Dawson Disease
-Progressive increase T2 signal and atrophy
several years after primary measles infection

168. T2 shows asymmetric high signal intensity lesions in both hemispheres , lesions in the
right thalamus and globus pallidus are noted

169. 2-Rasmussen’s Encephalitis :
-Progressive neurological deficits and intractable
seizures in children with progressive atrophy of the
involved hemisphere with large ventricle
-Increased T2 signal and atrophy in one cerebral
hemisphere
-N.B. :
*Notice that , opposed to hemimegalencephaly , the
smaller hemisphere is the site of abnormality and the
lateral ventricle is larger in the smaller hemisphere

170. Axial FLAIR and coronal T2WI show atrophy of the left cerebral hemisphere with
enlargement of the lateral ventricle

171. T1 & T2 shows prominent sulci , dilated lateral ventricle and hemiatrophy on
the left

172. Axial brain CT scan showing dilated left lateral ventricle and prominent left
sulci , in keeping with left hemiatrophy

173. T2 shows dilated left cerebral sulci and dilated left lateral
ventricle

174. Rasmussen’s Encephalitis (LT side) Hemimegalencephaly (RT side)

175. 7-Congenital CNS Infections :
a) Etiology
b) Radiographic Features

176. a) Etiology :
1-TORCH :
TOxoplasmosis (second most common)
Rubella
CMV infection (most common)
Herpes simplex
2-Other :
HIV infection
Syphilis
Varicella

177. b) Radiographic Features :
1-CMV Infection : (PV)
-Periventricular calcification : thick and chunky
-CT is adequate for diagnosis in 40%-70% of cases with
typical calcifications , however , calcifications may be
in atypical locations such as basal ganglia
(calcification generally appears faint and punctate , a
characteristic that helps distinguish basal ganglia
calcification due to congenital CMV infection from
that due to other causes which tends to be more
florid) or subcortical regions

178. -At MR , calcification appears as areas of low signal
intensity on T2-weighted images , this appearance is
especially evident on T2* weighted gradient-echo
images which are highly sensitive for depiction of
intracranial calcification
-Neuronal migration anomalies , especially
polymicrogyria
-Infection acquired during first two trimesters causes
congenital malformations , whereas infection in the
third trimester manifests as destructive lesions

182. (a) Axial unenhanced CT shows periventricular calcification (arrow) and
cerebellar atrophy (arrowhead) , (b) Axial unenhanced CT shows basal
ganglia and thalamic calcification (arrow) as well as ventriculomegaly with
severe generalized loss of volume

183. T2 , calcifications (arrow)

184. Atypical location , BG

185. With lissenencephaly

186. Diffuse pachygyria (arrows) , ventriculomegaly and white matter
lesions (arrowhead)

187. Right frontal focal polymicrogyria (arrows) , ventriculomegaly
and white matter lesions (arrowheads)

188. Diffuse increased signal intensity of white matter , a finding
indicative of delayed myelination

189. 2-Congenital Toxoplasmosis : (B&P)
-Basal ganglia and Parenchymal calcification
(diffuse) , intracranial calcifications may
regress or resolve over time in cases of
treated toxoplasmosis
-Hydrocephalus
-Chorioretinitis
-Migrational anomalies & encephalomalacia

190. Disappearing calcification in congenital toxoplasmosis , (a) unenhanced axial images of
the brain in a 12 month old infant shows ventricular enlargement , (b) CT at 4
years of age show that brain calcification is lessening over time

191. 3-Rubella :
-Microcephaly
-Basal ganglia and parenchymal calcifications
-Atrophy

192. Punctate calcifications of the basal ganglia (arrow) and low
attenuation of the white matter

193. 4- HSV-2 :
-Multifocal GM and WM involvement
-Hemorrhagic infarction , consider this diagnosis in a neonate who
presents in the second or third week of life with diffuse brain
edema and leptomeningeal enhancement
-Neonatal herpes encephalitis causes widespread MR imaging
signal abnormalities that are hypointense on T1 and
hyperintense on T2
-Neonatal herpes encephalitis usually involves the periventricular
white matter and spares the temporal and inferior frontal lobe
associated with adult herpes infection

194. (a) T1 shows area of hypointensity in white matter of left temporal-occipital
region , two small areas of hemorrhage involve gray-white junction , (b)
T2 shows hyperintensity in involved white matter

195. 5-Congenital HIV (Primary HIV Encephalitis) :
-Diffuse atrophy
-Basal ganglia calcification after 1 year

196. Progressive mineralizing vasculopathy of the basal ganglia

197. 8-AIDS :
-Central nervous system involvement in HIV is
the result of one of four mechanisms :
1-Direct Consequence of the HIV virus
2-Opportunistic Infections
3-Neoplasms in the Immunocompromised Host
4-Treatment / Drug Related Complications

198. 1-Direct Consequence of the HIV virus : AIDS
Dementia Complex
-HIV encephalopathy : See before
2-Opportunistic Infections :
a) Viral
b) Fungal
c) Protozoai
d) Bacterial

199. a) Viral :
1-CMV Encephalitis : See before
2-PML : See before
b) Fungal :
1-Cryptococcus :
-See Fungal Infections
2-Aspergillus & Candida :
-See Fungal Infections
-Rare in HIV , commoner in other immunocompromised
groups , e.g. bone marrow transplant recipients

200. c) Protozoai : (Toxoplasmosis)
-See before
d) Bacterial :
-Typical pyogenic infections
-T.B. :
Tuberculous meningitis with leptomeningeal
thickening , hydrocephalus , perforating vessel
infarcts , cerebritis & abscess

201. 3-Neoplasms in the Immunocompromised
Host:
-Lymphoma
-See Brain Tumors

202. 4-Treatment / Drug Related Complications :
-Immune reconstitution inflammatory syndrome
(IRIS) is the phenomenon of paradoxical
deterioration of an AIDS related illness following
initiation of highly active anti-retroviral therapy
(HAART)
-IRIS has been described with several opportunistic
pathogens , including TB , CMV , PML and
cryptococcosis as well as Kaposi sarcoma
-The imaging features may mimic worsening on the
underlying condition or be atypical

203. IRIS in a patient with biopsy-proved PML (a) T2 shows hyperintensity in the
bilateral (right greater than left) periatrial white matter , (b) T1+C reveals
diffuse patchy enhancement in the region of the T2 hyperintensity ,
(c) FLAIR obtained 2 weeks later demonstrates progression of the T2
hyperintensity with an increase in mass effect , (d) T1+C reveals
progression of the patchy enhancement in the 2-week interval

204. 9-Prion Infection : Creutzfeldt-Jakob Disease
(CJD)
a) Definition
b) Types
c) Location
d) MRI Findings

205. a) Definition :
-CJD is a transmissible fatal neurodegenerative disorder
caused by prions
-Diagnosis is by EEG & detection of 14-3-3 protein in
CSF
b) Types :
-There are four main subtypes: sporadic , familial ,
iatrogenic and variant CJD with the latter being
associated with mad cow disease
c) Location :
-The cerebral cortex and basal ganglia typically being
involved

206. d) MRI Findings :
-Typical MRI appearance is cortical ribboning which
describes ribbon-like FLAIR hyperintensity &
restricted diffusion of the cerebral cortex , the basal
ganglia & thalami are also involved , there is often
sparing of the motor cortex
-Pulvinar sign or hockey stick sign = typical bilateral
lesions in the pulvinar nuclei of the thalamus
(dorsomedial thalamus)
*Restricted diffusion seen at diffusion weighted MR
imaging is attributed to spongiform neuronal
degeneration and is more sensitive than T2 imaging
findings in detecting CJD , especially for cortical
lesions

207. FLAIR (top row) , DWI (bottom row) show diffusely increased FLAIR signal
with restricted diffusion in the cerebral cortex , basal ganglia &
dorsomedial thalamus , there is relative sparing of the motor cortex (red
arrows) , a hockey stick sign is visible on the 1st
FLAIR image (yellow
arrows)

208. Hockey stick sign

209. (a) T2 & (b) DWI show bilaterally symmetric areas of T2 prolongation and
restricted diffusion in the medial pulvinar nuclei of the medial thalamus
(pulvinar sign or hockey stick sign) (arrows)