Imaging of CNS infections

Imaging of CNS infections
DR MILI DUTTA


protocol
 Axial T1W
 Axial T2W TURBO
 Axial

FLAIR/Coronal
 Coronal/sag T2W
 CE—TIW
TIW Same parameter settings pre/post contrast
 3 D MP-RAGE(GRE) –THIN SLICES/ANY
PLANE/GOOD GREY WHITE DIFF


DWI
V

SENSITIVE TO VENTRICULITIS
 ABSCESS VS TUMOR


T2w/flair
 Infarct
 Edema
 Capsular

rim
 Perivent--FLAIR

T1w/c
 Meningeal
 Effusion

vs empyema
 Choroid plexitis—diff on FLAIR/DWI
because BRIGHT intravent contents
make it diff to detect
 Comparison of MRI Sequences to Detect
Ventriculitis AJR 2006; 187:1048-1053


TUBERCULOSIS


starts subpial / subependymal cortical focus (Rich focus),

GRANOLOMA ERODES INTO SAS LEPTOMENINGITIS

OBSTRUCTS FORAMEN
LUSHAKA/MAGENDIE—
OBSTRUCTIVE HYDROCEPHALUS

NON OBS

GRANULOMA
ABSCESS
CEREBRITIS

PACHYMENINGITIS

VASCULITIS (THALAMOSTR
//THALAMOPERFORATE
INFARCT


CT
 CECT--leptomeningeal

and basal cistern

enhancement.
 EPENDIMITIS- linear perivent enhancement
 VENT DIL (eg, third and fourth vent) due to
hydrocephalus
 low-attenuating focal infarcts deep gray-matter
nuclei, deep white matter, -due tovasculitis.
 Parenchymal cerebritis – hypoatt/ min
enhancement.
 Parenchymal tuberculomas
--. Noncaseating granulomas are homogeneously
enhancing lesions
-- Caseating granulomas are rim enhancing
--miliary pattern with multiple tiny nodules scattered
throughout the brain.
All surrounded by hypoattenuating edema.


MR

T1W--prominent leptomeningeal and basal cistern enhancement.

ependymitis, linear periventricular enhancement.
 Ventricular dilatation due to hydrocephalus
 . Deep gray-matter nuclei, deep white matter, and pontine infarctions
resulting from vasculitis are hyperintense on T2-weighted images.
 DWI -- early ischemic lesions when T2 N The primary differential
diagnoses are fungal meningitis, bacterial meningitis, carcinomatous
meningitis, and neurosarcoidosis.
 Parenchymal cerebritis hyperintensity with little or no enhancement
on T2-W
 tuberculomas hypo/HYPER on T2-weighted images.
 Noncaseating granulomas homogeneously enhancing//. Caseating
granulomas are rim enhancing. //miliary pattern with multiple tiny,
enhancing nodules scattered throughout the brain. -- surrounded by
hyperintense edema on T2-weighted images. The differential
diagnoses include fungal infections, bacterial infections,
neurocysticercosis, and cerebral metastases.
 MRS(single-voxel )TO D/D neoplasms.
-- elevated fatty-acid. Due to necrosis of the waxy walls of mycobacteria
within the granuloma
--. The lactate peak -- anaerobic glycolysis



INCREASED LACTATE,
DECREASED NAA,CHOLINE


THICK WALLED ABSCESS

MULTIPLE ENHANCING TUBERCULOMAS


vasculitis thalamoperforating a –
infarct basal ganglia/int capsules


Low SI rim (free oxygen radicals DUE TOinflammatory
process decrease T2 values +vasogenic edema
TUBERCULOMA



references
 Tuberculosis,

CNS: Peter D Corr et al
www.emedicine.com
 www.aids-images.ch


INTRAMEDULLARY
TUBERCULOMA


Brain abscess

Brain Abscess - pathology
 Location
 temporal

> frontal > other lobes

 >10%

are multiple
 Stages - based on histologic findings
 1.

Early cerebritis - poorly demarcated from
surrounding brain
 2. Late cerebritis - reticular marix (collagen
precursor) and developing necrotic center
 3. Early capsule formation - neovascularity,
necrotic center, developing capsule
 4. Late capsule formation - collagen capsule,
necrotic center, gliosis surrounding capsule


Abscess – MRI presentation
 MRI

presentation also varies with capsule
formation
 Early Cerebritic stage – hyperintense in T2 with
poor contrast enhancement on T1.
 Later Cerebritic Stage – central region of necrosis

is hyperintense to brain on T2, rim is isointense to
mildly hyperintense on T1. The capsule
enhances with contrast.
 Early and Late Capsule Stages – Capsule is
easily visible on unenhanced scans as a well
deliniated isointense to slightly hyperintence ring
with becomes hyperintense with contrast on T1.
Capsule is hypointense on T2


Abscess – CT presentation
 CT appeareance

dependent on stage
 Cerebritic stage – thick diffuse ring of
enhancement, further diffusion on contrast into
central lumen or lack of decay of contrast on
delayed scan 30-60 minutes later.
 Capsular stage – faint rim present on pre
contrast CT. (Necrotic center with edematous
surrounding brain makes the collagen capsule
easier to see.). Thin ring on enhancement and
there is decay of enhancement on delayed
scans.



Multiple abscesses in a 6 year
old

Subdural Empyema - evaluation
 CT of

head both with and without contrast
 LP - hazardous - risk of transtentorial
herniation
 Location 
convexity 70-80%

falcine 10-20%
 32/10,000 autopsies


Mixed Abscess Location