RING ENHANCING LESIONS IN BRAIN

SPEAKER : DR KOLLI DINESH(PG )

GMC SRIKAKULAM
 DEFINITION : Cerebral ring-enhancing lesions
• -area of hypodensity (CT) or hypointensity [MRI] of brain
tissue surrounded by a rim of enhancing tissue after contrast
injection.
• The etiologies
• infectious,
• neoplastic,
• post-treatment,
• demyelinating, and vascular causes.
 Cerebral ring enhancing lesions (mnemonic)
• T :Tuberculosis
• N : Neurocysticercosis
• M: metastasis
• A: abscess
• G: glioblastoma
• I: infarct (subacute phase),inflammatory
• C: contusion
• A: AIDS-related CNS disease (e.g. toxoplasmosis, cryptococcosis)
• L: lymphoma (this appearance is more common in immunocompromised)
• D: demyelinating disease (classically incomplete rim of enhancement)
• R: radiation necrosis or resolving hematoma
 INFECTIOUS
• TUBERCULOMA
• PYOGENIC ABSCESS
• NEUROCYSTICERCOSIS
• Echinococcus
• Toxoplasmosis
 INFECTIOUS CAUSES :
• Tuberculoma
• CNS TB –spread due to hematogenous route
Mycobacterium TB.
• Pathologic manifestations
- Acute/subacute TB meningitis (TBM) constitutes 70-80%
-second MC manifestation -focal parenchymal infection with
central caseating necrosis (TB granuloma or tuberculoma).
-The least common -CNS TB is abscess.
 1)Tuberculoma
• space-occupying masses of granulomatous tissue.
• Site -frontal and parietal lobes and basal ganglia.
• size. majority -small (less than 2.5 cm), and the "miliary"
nodules-few millimeters in diameter.
• "Giant" tuberculomas - 4-6 cm.
CLINICAL FEATURES – Seizures, headache,focal neurological
deficit
 RADIOGRAPHIC FEATURES
CT FINDINGS
• Hypo to isodense lesions are seen with edema and necrosis
appearing as a low attenuating area on CT scan .
• Organised granuloma – there may be high attenuation,contrast
enhancement or ring enhancement with variable degree of edema
• Enhancement is variable, ranging from small punctate foci to
multiple rim enhancing lesions.
• Mild to moderate round or lobulated ring-like enhancement with a
non enhancing center is the most typical pattern
• Calcification in chronic cases
 Contrasted CT -multifocal well defined ring enhancing lesions
NECT shows multiple lesions in the brain. with central hypodensity scattered throughout the brain.
A)NECT scan in a patient with CNS TB shows two calcified healed granulomas .
B)CECT scan in a 6y immunocompetent boy shows multiple small punctate-
enhancing tuberculomas .
• MRI
• T1 hypointense and
• T2 hypointense/isointense.
However, T2 hyperintensity -central liquified caseating material .
• DWI
Solid caseating tuberculomas do not restrict on DWI although liquefied foci may
restrict
• T1+C
Enhancement pattern is usually ring-shaped but a mass like or conglomerate lesions
may be seen.
• Large lipid peak(1.3) on MRS
41 years patient with
seizures.
T2WI (a) hypointense lesion
with extensive surrounding
edema in left frontal lobe.

post-contrast T1WI (b)

showing heterogeneous
enhancement of the lesion,
DWI (c) no restricted
diffusion. Findings
suggestive of solid
caseating
Tuberculoma.
Post-contrast T1WI (d) and
T2WI (e) 1 year post ATT
demonstrates complete
resolution of the lesion
T2WI- T1 C+ -additional lesions with punctate, ring
multifocal tuberculomas as hypointense foci surrounded enhancement
by edema
Axial T2WI shows
hypointense caseating
tuberculomas and edema . T1 C+ FS scan demonstrates both solid NAA -2.03,LIPID LACTATE 1.33
Central liquefaction is
hyperintense and thick rim enhancement.
a 57 years patient with new onset
altered sensorium. Postcontrast
T1WI (a,b,c), DWI (d) and T2WI
(e,f) -numerous small ring and disc
enhancing lesions diffusely
scattered in the bilateral cerebral
hemispheres, thalami, brain stem
and cervical spinal cord.
No restricted diffusion within the
lesions.
Demonstrate central T2
hypointensity with significant
perilesional edema

MILIARY TB
 19-year-old man with
immunosuppression after bone
marrow transplant and a history
of disseminated pulmonary
tuberculosis. demonstrate
multiple tuberculous granulomas
at different stages

Axial T2-weighted image (a), axial contrast-

enhanced T1-weighted image (b), and axial
ADC map (c)

A subcortical noncaseating tuberculoma -right temporal lobe shows homogeneous

enhancement with peripheral vasogenic edema
left occipital lobe, there is a lesion with central liquefaction
(arrow) that is compatible with a tuberculoma.
 Tubercular abscess
• infrequent pattern of presentation-less than 10% of cases
• Mc immunocompromised patients ,extremes of age.
• C/F -focal neurological deficits, fever, headache, and features
of raised ICT. Clinical progression is usually faster
 Tubercular abscess in the right basal ganglia of a 25-year-old woman.A well-defined hyperintense lesion is seen with
a hypointense wall on axial T2 (A), which shows ring enhancement on postcontrast T1 showing diffusion restriction

G. Luthra et al. AJNR Am J Neuroradiol 2007;28:1332-1338

©2007 by American Society of Neuroradiology

T1WCE shows an irregular
hypointense lesion with a thin
rim of peripheral
enhancement.

(T1IR axial) shows the lesion

to by hypointense.
The lesion shows diffusion
restriction on C (DWI axial)
heterogeneous in signal
intensity on D (T2W axial)
 2. PYOGENIC ABSCESS
• localized infection of the brain parenchyma-life-threatening disease
entity.
• Streptococcus species ,Staphylococcus aureus, and Pneumococci.
• Enterobacter species like Citrobacter -neonates
• Most abscesses are caused by hematogeneous spread
• predisposing factors-
• meningitis, uncorrected cyanotic heart disease, sepsis, suppurative
pulmonary infection, paranasal sinus or otomastoid trauma or
suppurative infections, endocarditis, and immunodeficiency or
immunosuppression states.
 RADIOGRAPHIC FEATURES
• CT FINDINGS
• Pre and post contrast
• Early stages Ill-defined hypodense mass on NECT
• Well-defined mass iso /hyper dense with strongly-enhancing
rim on cect.
• Late stages -Wall thickens, cavity and edema reduce
 •CECT scans show complete, well-delineated
NECT scans show large, welldefined rim enhancement ..
lesion with hyperdense rim and a •wall defect with adjacent area of new
hypodense center cerebritis
• MRI
• central part of the lesion -T1 hypointense and T2 mildly hyperintense ,no
suppression on FLAIR sequence.
• Peripheral ring enhancement -smooth and thin on T1+C with the wall
mostly being T1 and T2 hypointense.
• One of the features of pyogenic abscess is restricted diffusion at the
abscess cavity, This is due to tightly packed cellular content within the
abscess cavity.
• marked surrounding vasogenic oedema with mass effect .
• If it ruptures -ventriculitis
These images
are of a 55-year
old male with
headache
T2WI in early capsule stage of abscess T1 C+ in the same case shows intense
-classic "double rim" sign enhancement of the well-developed
with hypointense outer rim and mildly abscess capsule.
hyperintense inner rim
DWI (L) and ADC in the same case MRS in another late cerebritis/early
capsule abscess amino acids (valine, leucine, isoleucine)
show that necrotic contents of the abscess
at 0.9 ppm , acetate at 1.9 ppm , lactate at 1.3 ppm st,
cavity restrict strongly, whereas the wall of the and succinate at 2.4 ppm.
capsule itself does not NAA AND CHOLINE DECREASED
 Axial T1 C+ FS
scan in a 65y man with a history of
dental abscess, headaches for 2-3
weeks shows a left frontal thick-
walled ring enhancing mass
A xia lT1 C +FS
sca n in a 6 5 ym a n w ith a
h isto ryo fd en ta la b sce,
h ea d a ch esfo r2 -3 w eks
sh o w sa left p o sterio r
fro n ta thl ick-w a led rin g en h a n cin g
m ass

Coronal T1 C+ FS
edema and mass effect on
the ventricle.

post treatment shows a

small residual enhancing
nodule
Follow-up T1 C+ FS
scan 1 year later shows
that only a
small Hypointense non
enhancing focus
 3. NEUROCYSTICERCOSIS
• Taenia solium. four stages.
Clinical features
• Seizures/epilepsy mc symptoms (80%)
• result of inflammation around degeneration cysts.
• Headache (35-40%) and focal neurologic deficit (15%)
• subarachnoid forms—can also cause cerebral vascular
diseases.
• cerebral infarction,TIAs, and cerebral hemorrhage.
 RADIOGRAPHIC FEATURES
• Vesicular (quiescent) stage.
CT shows a smooth thin-walled cyst -isodense to CSF.
• no edema ,no enhancement on CECT.

MR -cyst is isointense with CSF on T1 and T2/FLAIR.

• The scolex is discrete, nodular, and hyperintense
("target" or "dot in a hole" appearance) and may restrict on DWI.
• Enhancement is typically absent.
• Disseminated or "miliary" NCC has a striking "salt and pepper brain"
appearance with no perilesional edema.
Vesicular stage. Unenhanced
CT
(A) shows a non-calcified
scolex (white arrow) and a
small parenchymal
calcification adjacent to the
cyst (nodular-calcified
stage) (black arrow).
Axial T1+C(B), T2-weighted
(C) and proton density (D)
MRI sequences. The cysts
have similar signal and
intensity to those of the
cerebrospinal fluid
• Colloidal vesicular stage (dying scolex).
• CT - Cyst fluid is hyperdense relative to CSF .
• ring enhancing capsule on CECT.
• Moderate to marked edema surrounds the degenerating dying larvae.
• MR-cyst fluid is mildly hyperintense to CSF on T1WI and that the scolex appears
hyperintense on FLAIR
• Moderate to marked surrounding edema -diffuse encephalitis.
• Enhancement of the cyst wall is typically intense, ring-like, and often slightly
"shaggy" .
• Restricted diffusion in the scolex and viscous degenerating cyst can be present
NCCT CECT
T1 T2 FLAIR T1 C+
Unenhanced (A and B) and
post-contrast (C) CT
images showing two
extraparenchymal lesions
in the left frontal lobe with
ring-like enhancement
after contrast
Calcified nodules in the convexity
(black arrows).
T2-weighted (D) and T-1
+C. The anterior one is in
the colloidal-vesicular
stage and the posterior in
the vesicular stage.
 STARRY SKY APPEARANCE

T1 T2 C+ T2 FLAIR
• Granular nodular (healing) stage.
• NECT mild residual edema. CECT demonstrates a progressively
involuting, mildly to moderately enhancing nodule.
• The cyst wall appears thickened and retracted
• Nodular or faint ring-like enhancement is typical
T1-weighted gadolinium-enhanced MRI
sequences (A and B) and

FLAIR sequences show small lesions with

nodular and ring-like hyperenhancement
located in left basal ganglia, left posterior
temporal lobe and both occipital lobes
(black arrows) with associated vasogenic
edema
• Nodular calcified (inactive) stage.
• CT - small calcified nodule without surrounding edema or
enhancement
• Shrunken, calcified lesions are seen as hypointensities on T1WI and
T2WI.
• Perilesional edema is absent.
• "Blooming" on T2* GRE is seen and may show multifocal
"blooming black dots" if multiple calcified nodules are present
• Quiescent lesions do not enhance on T1 C+.
 Echinococcosis

• Infection by Echinococcus is called echinococcosis.

• Two species of Echinococcus tapeworms, E. granulosis (EG) and
• E. multilocularis/alveolaris (EM/EA), -human CNS infections.
• EG infestation is also called hydatid disease or hydatid cyst
(HC). Infection with EM/EA is also known as alveolar
echinococcosis.
 Imaging

CT.
• large, unilocular, thin-walled cyst without calcification, edema,
or enhancement
• Occasionally, a single large cyst will contain multiple "daughter
cysts"
• MR –
• cyst fluid is isointense with CSF on T1WI and T2WI.
• Sometimes a detached germinal membrane and hydatid "sand"
• EA consists of numerous irregular cysts that—unlike HC—are
not sharply demarcated from surrounding brain -enhance on
contrast
Axial T1WI
shows a unilocular
hydatid cyst .

T2WI
in the same patient
the typical
three-layered cyst
wall
CECT scan shows
a multiloculated hydatid
cyst that contains
multiple "daughter
cysts."
T1WI, FLAIR,
DWI, and ADC (clockwise
from top left corner)
shows a hydatid cyst
with detached germinal
membrane and hydatid
"sand"
Surrounding edema and
mass effect are minimal
 Toxoplasmosis
• Mc opportunistic infection and overall cause of a mass lesion in
patients with HIV/AIDS.
• Toxoplasma gondii
• Site -basal ganglia, thalami, corticomedullary junctions,
and cerebellum.
• Multifocal lesions mc than solitary ones.
• Lesions are small -2-3 cm.
 Imaging

• CT Findings.
• NECT -multiple ill-defined hypodense with moderate to marked
peripheral edema
• CECT- Mc -Multiple punctate and ring-enhancing masses
Enhancement on is closely correlated to CD4 count. under 50,
enhancement is absent or faint.
• Enhancement becomes more pronounced as the CD4 increase
33y HIV-positive man in the ER
with altered mental status shows
hypodense masses in the left basal
ganglia and frontal lobe with marked
peripheral edema.
 MR Findings
• T1WI -hypointense mass sometimes mild peripheral
hyperintensity -coagulative necrosis or hemorrhage.
• T2WI -Alternating concentric zones of hyper and hypointensity
with marked perilesional edema .
• central T2 hyperintensity-necrotizing abscess.
• As abscess organizes- isointense relative to white matter.
• Perilesional hyperintensity represents edema with
demyelination.
T1 C+
• One or more nodular and ring-enhancing masses
• A ring-shaped zone of peripheral enhancement with a small
eccentric mural nodule represents "eccentric target" sign
• Nodule-concentrically thickened vessel
• rim enhancement is caused by an inflamed vascular zone that
borders the necrotic abscess cavity.
• MRS findings are nonspecific and often show a lipid-lactate
• peak.
 33y 33y HIV-positive
HIV-positive man in the ER man in the ER
with altered mental
status with altered mental
status
 NEOPLASTIC CAUSES
• 1) GLIOBLASTOMA :
• high-grade astrocytoma
classified as primary or secondary (arising from a low-grade
astrocytoma).
• Most primary glioblastomas are IDH wild-type whereas
secondary glioblastoma is more likely to have IDH–mutant status.
• Peak age = 45 years
Pathology
• Similar to IDH-wild-type but less palisading necrosis
• WHO grade IV
• Glioblastomas -unilocular complex, multilocular, thick walled,
ring-enhancing masses.
• large in size
• location deep white matter.
• cross the midline by infiltrating the white matter tracts of the
corpus callosum
• prominent neovascularity with abnormal blood-brain barrier
 RADIOGRAPHIC FEATURES
MRI
• T1 hypointense and T2 hyperintense,
• more heterogeneous -hemorrhage or central necrosis and the
outline of the lesion is more irregular.
• Focal restricted diffusion may be seen within the lesion
• T1+C -Irregular ring enhancement is a feature of glioblastoma,
often associated with a thick enhancing rim
T1 and T2 show a parietal heterogeneous mass with extensive perilesional
edema.
T1 post-contrast image demonstrates ring enhancement with thick irregular wall
and a shaggy inner margin.
T1, T2 and FLAIR
show a large
mass with
heterogeneous
content and
perilesional
edema.
T1 post-contrast
weighted image
(D) reveals ring-
enhancement
with irregular
wall
 2 . BRAIN METASTASIS
• Metastases are secondary tumors that arise from primary
neoplasms at another site.
• 10 times mc than primary malignant CNS tumors
• Common tumors that metastasize to the brain
• lung cancer,
• malignant melanoma,
• renal cell carcinoma,
• breast cancer, and colorectal carcinoma.
Brain metastasis can be solitary or multiple.
• Routes of Spread-hematogeneous dissemination
• Location
• The brain parenchyma mc (80%),
• skull and dura (15%).
• Diffuse leptomeningeal (pial) and subarachnoid space
infiltration is-5% of all cases.
• Size and Number- few millimeters and 1.5 cm.
50% are solitary lesions and 50% are multiple.
 RADIOGRAPHIC FEATURES
• CT findings
PRECONTRAST
• iso- to slightly hypodense relative to gray matter hyper (melanoma)
• edema is the most striking manifestation of metastases
• intratumoral hemorrhage. calcification is rare
CECT
• Uniform enhancement
• Solid, punctate, nodular, or ring patterns can be seen.
Axial NECT -
63y woman with known
breast carcinoma shows a
few scattered bifrontal
hyperdensities .

CECT
enhancing metastases,
most of which were
isodense and completely
invisible on the
precontrast study
 NECT in a 57y
woman in the ER with
seizure and altered
mental status shows
multiple patchy and
confluent hypodensities
NECT in a 57y
woman in the ER with
seizure and altered
mental status shows Emergency MR obtained
multiple patchy and
confluent hypodensities to "look for stroke.“
T1 C+FS shows multiple
enhancing nodules -cause
for the edema.
T1WI
• • Most metastases: iso- to slightly hypointense
• • Melanoma metastases: hyperintense
• Hemorrhagic metastases: heterogeneously hyperintense

T2/FLAIR
• Varies with tumor type, cellularity, hemorrhage
• Most common: iso- to mildly hyperintense
• Can resemble small vessel vascular disease
T1 C+
• Enhancement can be uniform or ring-shaped and the wall of ring-enhancing lesions is often
thick and irregular.
• Central necrosis may be seen within the tumor, and no restricted diffusion can be seen
within the necrotic region .
• Solid, punctate, ring, "cyst + nodule"
DWI
• Variable; most common: no restriction
• Highly cellular metastases may restrict
MRS
• Most prominent feature: lipid peak
• Elevated Cho, depressed/absent Cr
Differential Diagnosis
• Most common: abscess
Less common
• Glioblastoma
• Multiple embolic infarcts
• Small vessel (microvascular) disease
• Demyelinating disease
• Multiple cavernous malformations
Mets from lung carcinoma in
an elderly
T2 hyperintensities,
T1 C+ FS show punctate, ring
enhancement on
Some show restrictionon DWI
T2WI shows infiltrating,
cystic, hemorrhagic lesion

T1 C+ FS shows
bizarre multiloculated
ring enhancement

Preop Dx was GBM; breast

mets found at surgery.
patient with metastatic
lung cancer.
T1W+C - extensive
enhancement of the vessels
making it difficult to detect the
metastases.
On the black blood
sequence the signal of the
blood in the vessels is
suppressed making the
recognition of the enhancing
metastases easier.
 POST-RADIATION CAUSE:
• Post-radiation changes may simulate the appearance of
residual or recurrent tumor.
• Pseudo progression and cerebral radiation necrosis are both
sequelae of radiation therapy of the brain.
• It appears as an enlarging irregular ring-enhancing lesion
mimicking disease progression whereas it actually represents
a change related to underlying cell death.
 MR perfusion scan, pseudo progression will show reduced
cerebral blood volume
MR spectroscopy of pseudo progression often shows reduced
metabolites and increased lactate peak.
• Stability or shrinkage of the lesion through interval follow-up
imaging
• The mass effect of the lesion will be lost, unlike pseudo
progression.
A patient with
metastatic melanoma
treated with
stereotactic
radiosurgery (27 Gy in 3
fractions) demonstrating lesion
enhancement without contrast.
(A) T1 pre-contrast
sequence demonstrating
that the melanin within
the tumor tends to
enhance.
(B) T1 post-contrast
sequence
 DEMYELINATING CAUSE :
Multiple Sclerosis :
• MC demyelinating diseases is multiple sclerosis.
• T1 hypo intensity and T2/FLAIR hyperintensity, with a predilection
for the calloso-septal interface.
• progress with longitudinal extension perpendicular to the lateral
ventricles, giving the typical “Dawson’s fingers” appearance.
• Post-contrast and DWI sequences are useful to detect active
lesions/plaque. Sometimes these active lesions may be quite large
and mimic a mass lesion..
• Active demyelinating lesions -special ring-enhancing pattern
seen in the demyelinating disease known as “open ring
enhancement , which means there is incomplete ring
enhancement . The enhancing edge represents an active
demyelinating process in those regions
32y man with severe
headaches following
a viral prodrome

Axial T1WI in a
multiple hypointense
lesions in the deep white
matter Note faint rim
of T1 shortening
around two of the
lesions.

(15-12B) FLAIR MR in
the
same case shows
multiple
round and ovoid
hyperintensities .
Sagittal FLAIR in
the same case
demonstrates the
triangle
shape of the
periventricular lesions
T1 C+ FS showed
irregular rim
enhancement of
Some but not all of
thelesions.
Patient proven to have
definite MS.
 VASCULAR CAUSE HAEMATOMA :
• Hypertensive intracranial haemorrhage MC of intracranial
haemorrhage.
• It typically affects the basal ganglia, thalami, cerebellum, and
pons.
• IN subacute phase or early chronic phase, thin peripheral
enhancement around the hematoma is often evident and may
mimic tumor mass lesion..
subacute hematoma
• T1 and T2 hyperintensity of the lesion.
• peripheral ring enhancement should be thin. Peri lesional
vasogenic oedema -not significant.
• A hemosiderin rim that is complete is often seen on T2-
weighted image and
• blooming artefact is noted on DWI sequence.
• MR perfusion -the cerebral blood flow will decrease in case of
subacute hematoma
Edema
• Extensive favours abcess
• Increased perfusion favours neoplasm
CENTRAL FLUID CONTENT
Restricted diffusion favours abcess
Absence of diffusion favours tumor with central necrotic
component (clasically mets)
• NUMBER
Similar sized lesionsat GW junction –mets or abcess
Irregular masswith adjacent secondary lesions within same
region of edema favours GBM
Small (<2cm lesions with thin walls with other calcific foci
suggests Neurocyticercosis
 REFERENCES

• Characteristics of Ring enhancing lesions in brain in correlation with MRI and

MR spectroscopy -Yashraj P Patil1,Chirag R Patel2*,Rajesh S Kuber3, Rubab Kaur
Sekhon.
• Differential diagnosis of intracranial ring-enhancing lesions: a practical approach
• Imaging findings in neurocysticercosis S. Sarria Estrada ∗, L. Frascheri Verzelli, S.
Siurana Montilva, C. Auger Acosta, A. Rovira Canellas
• Magnetic resonance imaging spectrum of intracranial tubercular lesions: one
disease, many faces
• TEXTBOOK OF OSB0RNE THANKYOU .!