Imaging features of meningeal infection of the brain

1. I sincerely thank my
colleague for providing
the slides to me

2. meningitis
ARCHANA BALA
I YEAR DMRD

3. THE MENINGES
The meninges are layers of
tissue that separate the skull
and the brain
•Develop from meninx
primitiva
•It consists of
1) Pachymeninx-Duramater
2) Leptomeninges-Arachnoid
& Piamater
Skull
Dura
mater
Arachnoid Layer
Pia Mater
Brain

4. DURAMATER:
• Dura- ‘durus’ meaning hard
• Outermost ,thickest ,toughest layer
• 2 layers – outer endosteal layer
inner meningeal layer- folds-Falx cerebri
Falx cerebelli
Tentorium cerebelli
Diaphragm sellae
• Two layers split to form venous sinuses

5. ARACHNOID & PIA MATER:
• Leptomeninges – ‘lepto’ – Slender
• Arachnoid – adjacent to inner surface of dura
thinner over convexities of brain
• Pia mater – extends into depths of sulci
• Pia & Arachnoid are joined by fine connective tissue septa
• Enclose the sub arachnoid space containing CSF
• Perivascular Virchow Robin spaces – subpial space

6. Patterns of meningeal enhancement

7. PATTERNS OF MENINGEAL ENHANCEMENT:
1)Pachymeningeal Or Dura- Arachnoid pattern
2)Leptomeningeal Or Pia- Arachnoid pattern

8. Pachymeningeal enhancement
• Dura enhances normally on contrast enhanced CT & MRI -
because of absence of Blood brain barrier
• Manifested against the inner table of cranial convexity ,dural
reflections of the falx cerebri, tentorium cerebelli, falx
cerebelli, and cavernous sinus
• Normal-only thin, linear, and discontinuous enhancement
• Pathological enhancement –is thicker-
Regular & Diffuse-
1) inflammation
2) intracranial hypotension
Irregular & Focal-
neoplasms such as meningiomas, metastatic
disease (from breast and prostate cancer), secondary CNS
lymphoma

9. DURA-ARACHNOID PATTERN

10. Pachymeningeal enhancement

11. Leptomeningeal Enhancement
• Enhancement of the pia mater or enhancement that extends
into the subarachnoid spaces of the sulci and cisterns is
leptomeningeal enhancement
• There is presence of Blood brain barrier
• Enhancement occurs when there is breakdown of BBB
pathologically
• Usually associated with meningitis

13. Meningeal enhancement on contrast enhanced CT & MRI
is nonspecific and may also be caused by
• Infectious meningitis
• Carcinomatous meningitis
• Reactive (eg, surgery, shunt, trauma)
• Chemical (eg, ruptured dermoid and cysticercoid cysts,
intrathecal chemotherapy)
• Inflammatory (eg, sarcoidosis, collagen vascular
disease
• Intracranial hypotension (CSF leak)
• Idiopathic hypertrophic cranial pachymenigitis

14. • Meningitis is the most common form of CNS infection
• Pachymeningitis-Obsolete now
Disesase of Pre penicillin era
Syphilis-secondary & tertiary stages
Inflammation of dura mater
• Mild forms of neuro syphilis still occurs that may go
unrecognized because of minimal symptoms and signs
MENINGITIS

15. • Leptomeningitis - Involves Pia mater , Arachnoid &
Sub arachnoid space
• It is a clinical & lab diagnosis
• Single most important test in diagnosis – CSF Analysis

16. MODE OF SPREAD
• Direct spread from without - skull fracture
penetrating wounds of scalp
spread from PNS mastoid
• Direct spread from within – Rupture of brainabscess,
tuberculoma
• Through Blood stream – Following Bacteremia
• Complicating Encephalitis & Myelitis – Poliomyelitis
• Other modes – Iatrogenic - Spinal Anaesthesia
VP Shunt

17. DIAGNOSIS : established by
1. History and physical examination
Fever, Headache, Seizures, Altered
sensorium , Neck stiffness
2. CSF Analysis

18. LUMBAR PUNCTURE –indispensable
investigation

19. ROLE OF NEUROIMAGING IN
MENINGITIS
• To exclude contraindications to Lumbar Puncture
• Detect Complications
Hydrocephalus
Subdural Empeyma
Cerebral Abcesses
Ventriculitis
Vasculitis - Infarction
•Repeat Ct – Failure of a patient with suspected viral
meningitis to improve within 48 hrs

20. CLASSIFICATION
INFECTIOUS
NON
INFECTIOUS
INFLAMMATORY
BACTERIAL
MYCOBACTERIAL
FUNGAL
ASEPTIC
SARCOIDOSIS
WEGENER’S
GRANULOMATOSIS

21. CATEGORIES OF MENINGITIS
INFECTIOUS MENINGITIS
1. Acute pyogenic meningitis
2. Acute lymphocytic meningitis
3. Chronic/Granulomatous meningitis

22. ACUTE PYOGENIC MENINGITIS
CAUSATIVE ORGANISMS:
Neonates - E.Coli
Listeria Monocytogenes
Group B Streptococci
Children < 7 yrs - H.Influenza
Children > 7 yrs – Neisseria Meningitidis
Adults - Streptococcus Pneumoniae

23. IMAGING IN BACTERIAL
MENINGITIS
• Chest X ray – to disclose area of abcess , pneumonitis
• X ray PNS ,Skull – to r/o Cranial osteomyelitis,
paranasal sinusitis, mastoiditis
NEUROIMAGING is the investigation of choice
• CT scan
• MRI with Gadolinium enhancement

24. IMAGING FEATURES
NECT
 Mostly normal
 Mild ventricular dilatation and subarachnoid
space enlargement
 Small ventricles may be seen secondary
to diffuse cerebral edema
 Effacement of basilar and convexity cisterns
by inflammatory exudates

25. Effacement
of Sylvian
cistern
Effacement
of Basilar
cisterns

26. Temporal horn
lateral ventricle
3rd Ventricle
4th Ventricle
DILATED

27. Dilated Lateral
Ventricles

30. CECT
 Marked curvilinear meningeal enhancement over
cerebrum (Frontal & Parietal lobes) –
LEPTOMENINGEAL ENHANCEMENT
 Obliteration of basal cisterns with intense
enhancement
 Interhemispheric and sylvian fissures also
show enhancement

31. Basilar cistern
enhancement

32. Intense
Leptomeningeal
enhancement

33. Post contrast Leptomeningeal enhancement

34. COMPLICATIONS
• 1) HYDROCEPHALUS
• Extensive fibrinopurulent exudates can obstruct the
subarachnoid space leads to EVOH
• Aqueductal obstruction leads to IVOH

35. Hydrocephalus

36. 2)SUBDURAL EFFUSION & EMPYEMA
• Benign subdural effusions – H.influenza
• Due to irritation of the dura by infectious agents or
its by-products or by inflammation of subdural veins
with loss of fluid and albumin into the subdural space
infection
Subdural
empyema

37. Subdural effusion
Crescentic extraaxial fluid collection that are similar to CSF,
frequently seen in the Frontal region , on both CT & MRI
Subdural
effusion

38. Subdural empyema-
• Crescentic / lentiform extraaxial fluid
• Collection that are hypodense on CT with intensely
enhancing surrounding membrane

39. 3) CEREBRITIS & ABSCESS
a. Early cerebritis (3-5 days)
b. Late cerebritis (5-14 days)
c. Early abscess (after 14 days)
d. Mature abscess (last for wk/months)

40. Cerebral Abscess

41. 4) VENTRICULITIS / EPENDYMITIS
• Rupture of a periventricular abscess (or)
Retrograde spread of infection from basal cisterns
• On Nonenhanced scans – Slightly increased density
in the region of affected ependyma
• On Contrast study – Uniform , thin ependymal
enhancement

42. Ependymal
Enhancement
Ventricular
Debris
Ventriculitis

43. 6) CEREBROVASCULAR LESIONS
• Most frequent intracranial complication
of bacterial meningitis in adults (37%)
• Develops in up to 27% of children with
tuberculous / complicated bacterial meningitis
• Imaging - Vessel wall irregularities , Focal dilatations,
Arterial occlusions , Venous infarcts

44. Vasculitis-
PEFFORATING VESSELS AT
BASE OF BRAIN
THROMBOSIS
INFARCTION

45. ACUTE LYMPHOCYTIC MENINGITIS
Viral in origin
• Enteroviruses(Echo/Coxsackie viruses)
• Mumps , EBV , Arboviruses
• Benign and self limited
• Symptoms less severe than bacterial
• Imaging – Usually normal unless coexisting
encephalitis occurs

46. CHRONIC/GRANULOMATOUS
MENINGITIS
More common - TUBERCULOSIS
Less common
Cryptococcosis
Coccidiomycosis ( endemic )
Mucormycosis (diabetics )
Aspergillosis (immunocompromised )

47. • Hematogenous spread from pulmonary,abdominal or
genitourinary TB
• Direct extension –rupture of tuberculoma into SA space
• Primarily very young and very old persons are affected
• Increased incidence in drug abusers and
immunocompromised patients
TUBERCULOUS MENINGITIS

48. CLINICAL FEATURES:
Adults-Chronic headache
Fever
Diabetes insipidus
Cranial palsy
Seizures
Meningismus
Lethargy
Children – Nausea , Vomiting , Behavioral
changes

49. PATHOLOGY:
Thick , gray gelatinous exudate that predominantly
involves the BASILAR CISTERNS
CSF ANALYSIS:
Decreased glucose
Increased protein
Lymphocytic pleocytosis

50. COMPLICATIONS
• Hydrocephalus
• Infarction -Involving
• Medial Lenticulostriate Artery (ACA) &
thalamoperforating arteries (PCA)
• Cranial nerve palsy(17-70%)-
Involving the second, third, fourth, and seventh
cranial nerves
• Atrophy

51. NEUROIMAGING:
NECT:
• Basal cisterns and Sylvian fissures have a density
similar to that of the adjacent brain due to the presence
of purulent exudate
• Extraventricular Obstructive hydrocephalus-obstruction
at level of basilar cisterns
• Infarction (20-40%) involving basal ganglia or internal
capsule
CECT:
• Intense enhancement of the basilar cisterns and
Sylvian fissures

52. CHRONIC TUBERCULOUS MENINGITIS
Isolated TB meningitis rare
5% of childhood bacterial meningitis
17.5% of all intracranial TB cases
Most patients have concomitant miliary
brain infection
11% of all patients have combined
parenchymal & meningeal lesions

53. NECT:
• “En plaque” dural thickening
• “Popcorn” like dural calcifications –
particularly around basal cisterns
CECT:
• May disclose abnormal meningeal
enhancement years after the initial
infection
• SEQUELAE of chronic meningitis – atrophy
and cerebral infarction may be striking

54. CT-
NECT-Appear as round or lobulated masses with low or
high attenuation
CECT-homogeneous or ring enhancement and have
irregular walls of varying thickness.
“Target Sign” (central calcification with surrounding
hypoattenuation and ring enhancement)-seen in 1/3rd
patients

55. • Usually associated with
tuberculous meningitis
• Appears at MR imaging
as multiple tiny (<2-mm),
hyperintense T2 foci that
homogeneously enhance
on contrast-enhanced
T1-weighted images
MILIARY CNS TUBERCULOSIS

56. THANK YOU