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CNS INFECTIONS. SOWMYA - Copy.pptx
1. IMAGING OF CNS INFECTIONS
MODERATOR : DR. C N PRADEEP KUMAR
PRESENTER : DR. SOWMYA JAGADISH
2. CONGENITAL / NEONATAL INFECTIONS OF THE
BRAIN :
CMV
TOXOPLASMOSIS
RUBELLA
H. SIMPLEX
HIV INFECTION
MENINGITIS :
AC. PYOGENIC MENINGITIS
AC. LYMPHOCYTIC MENINGITIS
CH. MENINGITIS
3. PYOGENIC PARENCHYMAL INFECTIONS
CEREBRITIS AND ABSCESS
COMPLICATIONS OF CEREBRAL ABSCESS
ENCEPHALITIS :
H. SIMPLEX ENCEPHALITIS
HIV ENCEPHALITIS & OTHER CNS INFECTIONS
IN AIDS
TUBERCULOSIS AND FUNGAL INFECTIONS :
CNS TUBERCULOSIS
FUNGAL INFECTIONS
PARASITIC INFECTIONS :
NEUROCYSTICERCOSIS
MISCELLANEOUS PARASITIC INFECTIONS
15. IMAGING FINDINGS ACCORDING TO TIME OF
INFECTION
1ST & EARLY 2ND TRIMESTER(BEFORE 18WKS)
Lissencephaly with thin cortex
Cerebellar hypoplasia
Ventriculomegaly
Delayed myelination & periventricular calcification
20. TOXOPLASMOSIS
Causative organism: Toxoplasma Gondii
2nd Most common cause of cong. CNS infections
Pathophysiology:
Multifocal scattered lesions in BG, periventricular white
matter & cortex.
No migrational disorder.
Non specific findings- atrophy, microcephaly &
hydranencephaly
Imaging: show typical triad of
Intracranial Calcification,
B/L Chorioretinitis &
Hydrocephalus
21.
22.
23. RUBELLA
PATHOPHYSIOLOGY:
Interferes with the cellular multiplication causing decreased
no of neurons, astroglia & oligodendroglia resulting in
impaired myelination
Brain abnormalities that can occur are meningoencephalitis,
vasculopathy, micrencephaly
Micrencephalia vera: rare entity brain is formed but markedly
small.
24. IMAGING FINDINGS
ULTRASOUND:
Subependymal cysts in caudate nucleus & striothalamic
region.
Echogenic foci in basal ganglia-mineralising vasculitis with
calcifications.
CT:
Microcephaly & parenchymal calcification
MRI:
Deep & subcortical white matter lesions-vascular injury &
ischemic necrosis.
Delayed myelination – insufficient no. of oligodendroglia.
25.
26. HERPES SIMPLEX
Neonatal HSV encephalitis is diffuse disease without
prelediction for temporal lobes and limbic system.
Early changes : meningoencephalitis with necrosis,
haemorrhage and microglial proliferation.
Late changes : atrophy with gross cystic encephalomalacia
and parenchymal calcifications
Severe : near total loss of brain substance with
hydranencephaly.
27. CT: Focal or diffuse white matter lucency. the relative
hyperdensity of the cortical grey matter appears accentuated.
Hemorrhagic infarction may occur.
diffuse atrophy & multicystic encephalomalacia are long term
sequelae.
MR: Hypo on t1 & hyper on t2/FLAIR. DWI
diffuse white matter edema is difficult to detect as neonatal
brain is largely unmyelinated(proton dens mr)
MRS: May show increased lactate & choline during acute period,
decreased NAA
IMAGING FINDINGS
28. T1WI shows multiple bilateral cortical, basal ganglia foci of T1 shortening
s/o subacute haemorrhage.
More cephalad scan shows additional areas of T1 shortening.
29.
30.
31. IMAGING FINDINGS:
CT
Cerebral atrophy(90%),
Calcification is typically bilaterally symmetrical mainly seen in
BG
Hemorrhage and infarction are known complications.
MRI
Reveals diffuse atrophy and abnormalities of the white
matter.
On T2W images areas of increased signal in peripheral & deep
cerebral white matter without associated mass affect.
Ectasia and fusiform enlargement of intracranial arteries.
Strokes with foci of restricted diffusion noted.
CONGENITAL HIV
37. ACUTE PYOGENIC MENINGITIS
ROUTES OF SPREAD:
Haematogenous, Local extension from contiguous infection ,
Direct implantation in skull.
PATHOLOGY:
Most imp. pathological feature is thick creamy purulent exudate
confined to basal cistern or completely filling the
subarachnoid space
38. IMAGING FINDINGS
NCCT: Mostly normal
Mild ventricular dilatation & subarachnoid space enlargement are early
abnormalities. Effacement of basilar or convexity cisterns by exudate is
also seen.
CECT: Enhancing exudate in sulci & cistern.
Low density areas related to perfusion alteration
MRI: T1WI – Exudate is isointense (dirty CSF). T2 & FLAIR- Exudate is
hyperintense and do not suppress on FLAIR.
T1WI with contrast-strong enhancement is seen
Diagnosis is basically by lab investigations & imaging is mainly to monitor
complications.
51. CEREBRITIS & ABSCESS
Cerebritis is earliest stage of purulent brain infection Abscesses evolve from
focal cerebritis
Hematogenous spread, from local infection (mastoid & sinus infection), may be
preceded by empyema or meningitis.
Corticomedullary junction is most common location
Frontal and parietal lobes are most frequent sites
4 stages pathologically
1. Early cerebritis : 3 to 5 days
2. Late cerebritis :10 to 14 days
3. Early capsule formation : begins at about 2 wks
52. 4 stages pathologically
1. Early cerebritis : 3 to 5 days
2. Late cerebritis :10 to 14 days
3. Early capsule formation : begins at about 2 wks
4. Late capsule formation : may last for weeks /mths
53. 1.EARLY CEREBRITIS
IMAGING FINDINGS
•NECT: Ill-defined hypodense subcortical
lesion with mass effect / may be normal
early
•CECT : +/- Mild patchy enhancement
• TlWI: Poorly marginated, mixed
hypointense/isointense mass
•T2WI: ll-defined hyperintense mass
54.
55.
56. LATE CEREBRITIS
IMAGING FINDINGS
o NECT: Central low density area; peripheral edema,
mass effect increase
CECT: Irregular peripheral rim enhancement
T1W1: Hypointense center, isointense/mildly
hyperintense rim
T2: Hyperintense center, hypointense rim; hyperintense
edema
57. EARLY CAPSULE FORMATION
NECT: Hypodense mass with moderate vasogenic edema and mass effect
CECT: Low density center with thin, distinct enhancing capsule
T1: Rim isointense to hyperintense o WM ; center hyperintense to CSF
T2: Hypointense rim.
58. LATE CAPSULE FORMATION
IMAGING FINDINGS
• Edema, mass effect diminish, Cavity shrinks, capsule
thickens, enhancement of capsule
• May be multiloculated and have "daughter abscesses
MRS: Central necrotic area may show presence of acetate,
lactate, alanine, succinate, pyruvate, and amino acids
66. NCCT:
Multiple areas of hypodensity particularly in bg & thalamus.
CECT:
Ring or nodular enhancement
MRI:
t2wi variable signal intensity in active lesion
target sign- central isointensity / hypointensity with
peripheral high intensity edema
POST GADOLINIUM: ring or nodular enhancement
OPPORTUNISTIC INFECTIONS IN HIV
TOXOPLASMOSIS
69. DD:1 LYMPHOMA
1.SITE
2. SIZE & NO OF LESIONS
3.HEMORRHAGE
4.MRS
5. MR PERFUSION
7. DW
6.PET/SPECT
2. TUBERCULOSIS
70. CONCLUSION
IN THE DIAGNOSIS OF CNS INFECTIONS COMINED
APPROACH IS NEEDED.
KNOWLEDGE OF EACH INFECTION IMAGING
FEATURES.
CSF ANALYSIS
BLOOD INVESTIGATIONS & SEROLOGY
BIOPSY
Axial section of NSG showing ventricular adhesions and lenticulostriate vasculopathy.
T1 weighted axial section showing ventricular adhesion in occipital horn of right lateral ventricle.
Branching basal ganglia and thalamic echogenic streaks
(lenticulostriate mineralising vasculopathy)
NCCT image axial section showing schizencephaly with periventricular calcification.
Axial NECT showing the intraparenchymal calcifications involving the cerebral cortex and subcortical white matter.
Axial T2 w shows delayed myelination and symmetric periventricular hyperintensities.
Widespread areas of hypoattenuation
T2W of the same infant after 1 month shows multicystic encephalomalacia with blood fluid levels and areas of ribbon like T2 shortening in the cortex is seen secondary to haemorrhage. More cephalad scan shows cystic encephalomalacia underlying foci of T2 shortening.
Atopsy specimen showing marked enlargement of ventricles with cystic encephalomalacia.
Coronal flair shows extensive cystic encephalomalacia
Generalised brain volume loss, enlargement of ventricles and subarachnoid spaces. Multiple foci of microglia, macrophages and mng cells can be seen.
Mineralising microvascular angiopathy with basal ganglion calcification are seen.
Bilateral symmetrical calcification in the basal ganglia.
Bilateral symmetrical calcification in the basal ganglia.
Cloudy csf fills the subarachnoid space, development of dense purulent exudate which covers the pial surface. The vessels within exudate may show inflammatory changes and necrosis.
NECT shows enlarged ventricles with blurring of margins, effaced suprasellar and interpeduncular cisterns.
Cect scan shows enhancing exudate filling the sylvian fissure and coating the surface of interpeduncular cistern.
Intense enhancement of the exudate as it covers the brain surfaces, extending into and filling the sulci.
Atopsy specimen shows the purulent exudate filling the sas and obliterating the sulci.
Flair scan shows hyperintensity covering the pial surface of all the convexity gyri.
T1 W C+ FS scan shows diffuse intense enhancement of the basal cisterns and sulci
Enhancement covers the pial surfaces of gyri and fills the convexity sulci.
Axial T1 C+ showing debris fluid levels in the lateral ventricles. Cerebral abscess adjacent to the ventricle can be noted.
DWI shows intense restriction of intraventricular debris and the cerebral abscess shows strong diffusion restriction.
Early stage. Infection is focal but not localised. Enencapsulated, edematous hyperemic mass of leukocytes and bacteria intermixed with patchy necrotic foci and petechial hemorrhages.
NECT shows an ill defined hypodensity with mild mass effect in right posterosuperior temporal lobe- resembles infarct
T1w shows an ill defined hypointense mass.
T2 w of the same patient shoes mixed iso and hyperintense mass
Dwi shows mild restricted diffusion at the periphery. And center of the lesion.- this is not usually seen in infarct.
The necrotic foci coalesce, forming a confluent core. The necrotic center is surrounded by poorly organised rim of inflammatory cells, macrophages, granulation tissue and fibroblasts.capillary proliferation and surrounding vasogenic edema become more prominent.
The necrotic core liquefies and granulation tissue around the rim gradually forms a well delineated collagenous capsule.. Vasogenic edema begins to decrease.
The central cavity gradually involutes and shrinks, collagen deposition further thickens the wall and surrounding vasogenic edema will disappear.
Axial T1 w image shows a predominantly hypointense masswith an incomplete slightly hyperintense rim
T2 w shows double rim sign with hypointense outer and hyperintense inner rim.
The rim is hyperintense on FLAIR. Moderate peripheral edema is present.
T1 c+FS shows the rim enhancement around the nonenhancing center of the mass.
DWI shows that the center of the lesion restricts strongly.
MRS shows aa(val, leu, iso) at 0.9 ppm, acetate at 1.9 ppm, lactate at 1.3 ppm and succinate at 2.4 ppm.
A. T2WI reveals a right parietal mass lesion with high signal intensity centrally and low signal intensity peripherally within the capsule. There is surrounding high-signal-intensity edema. Two smaller high signal lesions are present on the left. B. Gadolinium-enhanced T1WI shows thin, smooth enhancement of all three lesions
The mass restricts strongly on DWI. ADC shows that the mass is very hypointense compared to the normal brain parenchyma confirming that the hyperintensity seen on DWI is true diffusion restriction. The hyperintensity surrounding the mass is edema.
Area of hypodensity seen in right basal ganglia region.
central isointensity / hypointensity with peripheral high intensity edema
