5. • Pathology
I. Cloudy CSF fills the subarchnoid spaces,
followed by development of variably dense
purulent exudate that covers the pial
surfaces.
II. Basal cisterns and subarachnoid spaces are
the most commonly involved by meningitis.
6. Imaging
• Imaging should be use in conjunction with
appropriate clinical and laboratory evaluation.
7. • CT findings
Non contrast CT
-mild ventricular enlargement with slightly
blurred margins.
- Cisterns and sulci appears effaced as they
become almost isodense with brain.
8. • Contrast enhanced CT.
Intense enhancement of inflammatory exudate
as it covers brain surfaces as it covers brain
surfaces extending into and filling the sulci.
25. • Late cerebritis.
Necrotic centre is surrounded by poorly
oraganised rim of inflammatory cells.
Begin at 4 days and last between 10 days to
2weeks.
26. • CT Findings.
NECT- better delineate central hypodense mass
with surrounding edema
CECT-Irregular rim enhancement.
31. • Early capsule
Necrotic core liquifies and proliferating
granulation tissue around the rim gradually
forms well delineated collagen capsule.
Stage around 2 weeks and may last for month or
two
35. 4. Late capsule
Central cavity gradually involutes and shrinks
Collagen deposition further thicken the wall.
This stage begins several weeks following
infection and last for several months.
37. Differential diagnosis
• Early cerebritis are poorly defined may mimic
cerebral ischemia or neoplasm.
• Ring enhancing lesions , the most common
differential is infection vs
neoplasm(glioblastoma or metastasis)
38. Ventriculitis
• A collection of purulent material in the
ventricle is more likely due to intraventricular
rupture of brain abscess.
• Risk is increases if abscess is deep seated,
multiloculated or close to ventricular wall.
39. • Imaging
CT findings
Debris level in the dependent part of occipital
horn together with periventricular hypodensity.
45. • Etiology
Mycobacterium tuberculosis complex
o Vast majority caused by M. tuberculosis
o Other mycobacteria(m. bovis) rare.
Neurotuberculosis is secondary to hematogenous
spread extracranial infection, most frequently in
the lung.
46. Pathology
CNS TB has several distinct pathological manifestations
• TB meningitis (70-80%)
Exudative, proliferative and necrotizing component in sub
arachnoid cistern.
• Tuberculoma (TB granuloma)(20-30%)
Focal parenchymal infection with central caseating
necrosis.
• Pseudoabscesses
Found in 20% of patients coinfected with TB and HIV
47. IMAGING
• TB meningitis
Non contrast CT findings
-blurred ventricular margins
-effacement of basal cisterns by hyperdense
exudate.
48. • Contrast enhance CT findings
-Intense enhancement of basilar meninges and
subarachnoid spaces.
49. • MRI findings
T1WI basilar exudates are isointense with brain
giving the apperance of dirty CSF.
52. • Vascular complications are common
complication of TBM
-flow voids of major arteries appears reduced.
-parenchyma adjacent to meningeal
inflammation may demonstrate necrosis.
-penetrating artery infarct with restricted
diffusion are common.
53. • Tuberculoma
Non contrast CT findings
-Isodense to slightly hyperdense round,
lobulated mass with variable perilesional
edema.
-Calcifications can be seen in healed ganuloma
57. • T1+C
Ring like enhancement with around the no
enhancing centre.
58. • MR spectroscopy
Helpful in characterizing and distinguishing the
tuberculomas from pyogenic abscess and
neoplasm.
A large lipid peak with abcesnce of other
metabolites and succinate is seen in 85-90%
cases
60. Neurocysticercsis
• Most common parasitic infection in the world.
• CNS lesions developed in 60-70% of patients
with cysticercosis.
Etiology
Pathology
Imaging
Differential diagnosis
62. • Pathology
four stages of NCC development and regression are
recognised.
Patients may have multiple lesions at different stage
of evolution.
1. Vesicular stage
2. Colloid vesicular stage.
3. Granular nodular stage.
4. Nodular calcified stage.
63. Imaging
• Vesicular stage
Viable larvae appears as translucent, thin
walled, fluid filed cystic lesion with eccentrically
located scolex.
64. • Non contrast CT
Smooth thin walled cyst that is isodense to CSF.
• Contrast enhanced CT.
No enhancement , no surrounding edema.
65. • MR findings
Cyst is isointense to CSF on T1WI, T2WI and
FLAIR.
Scolex is hyperintense.
67. • Colloid vesicular stage.
Larvae begin to degenerate
Cyst fluid become thick and turbid
A fibrous capsule develops and perilesional
edema becomes prominent.
68. • Non contrast CT Findings
Cyst fluid is hyperdense relative to CSF.
