Approach to ring

enhancing lesion CT/MRI

Speaker. Dr. Vivek kumar gupta

Moderator .Dr Deepak Sachan(asst. prof.)

Dr vivek chaudhary (SR)

Ring Enhancing lesions

Lesions having
hypodense centre
with hyperdense
sorrounding on
contrast CT/MRI
scan of the brain.
Ring Enhancing lesions
Causes
A) Infectious Neurocysticercosis (NCC)
Tuberculoma
Brain abscess
Toxoplasmosis
Fungal granuloma
Syphilitic gumma
Nocardia
Actinomycosis
Cryptococcus neoformans
Candida Albicans
Aspergillosis
Mucoromycosis
B) Neoplastic Lymphoma
Glioma
Metastasis

C) Degenerative Demyelinating plaques

Neurocysticercosis
 Most common CNS parasitic infection (60-70%)
 Endemic in Central South America, Parts of Asia, Eastern
Europe, in developed countries due to immigrants from
endemic areas.
Life cycle
Mode of infestation
Contaminated food or water
with eggs of pork tapeworm

Oncospheres in Gut
(Primary larvae)
Intestinal mucosa

Circulatory system

Brain Muscle Eye

Neurocysticercosis
Location
1) Parenchymal (MC ) in corticomedullary region
2) Extraparenchymal
a) In ventricle
b) In basal cistern(racemose cysticercosis)

Right frontal inflammatory

granuloma
Pathologic stages of parenchyma
cysticercosis
Vesicular stage
First stage, cysticercus consist of a thin capsule
that surrounds a viable larva and clear fluid.
IInd pathological stage
Vesicular Colloidal stage
Dead larvum degenerates,
the cystic fluid becomes
turbid, cyst shrinks, capsule
thickens.
Degenerating larvae release
metabolic products resulting
host inflammatory response
(surrounding edema).
Pathologic stage IIIrd
Granular nodular stage
Cyst retracts thickens and calcifies.
IVth pathological stage
Nodular calcified stage

Granulomatous lesion has

contracted small calcified
nodule without
enhancement effect is
visible on CT.
Diagnosis criteria advised by de brutto et al,2001

1. Absolute criteria
2. Major criteria
3. Minor criteria
4. Epidemiological criteria
Diagnosis of Neurocysticercosis
Neuroimaging is the mainstay of diagnosis
Absolute Diagnostic Criteria
 Histological demonstration of the
parasite from biopsy of brain.
 Cystic lesions with scolex on CT or MRI
 Direct visualization of subretinal
parasite by fundoscopy.
Diagnosis of neurocysticercosis
Major Criteria
 CT or MRI showing cystic lesions without scolex,
enhancing lesions or typical brain calcifications.
 Positive serum immunoelectrotransfer blot(EITB)
for detection of anticysticercal antibodies.
 Resolution of cysts after antiparasite therapy.
 Spontaneous resolution of small single enhancing
lesions.
Diagnosis of neurocysticercosis
Minor Criteria
 CT or MRI showing hydrocephalus or abnormal
enhancement of meninges.
 Seizures, focal signs, intracranial hypertension and
dementia.
 Positive CSF ELISA for anti cysticercal antibodies.
 Cysticercosis outside the CNS.

Epidemiologic Criteria
 Evidence of household contact with Taenia solium
infection.
 Individual coming from living in an endemic area,
 History of travel to an endemic area.
Diagnosis of neurocysticercosis
Definitive
 Presence of one absolute criterion (1/3).
 Two major (2/4) + one minor (1/4) and + one
epidemiologic criteria (1/3).
Probable
 Presence of one major + two minor criteria.
 One major + one minor and + one epidemiologic
criteria.
 Three minor + one epidemiologic criteria.
Can CT differentiate between tuberculoma
and Neurocysticercosis
Not with certainty, factors may be taken into account are-
NCC TUBERCULOMA
Location Parietal (subcortical Basal regions in posterior
interface), temporal, fossa in younger children
Frontal, Occipital
Number Single or more Often multiple, satellite
lesion
Size Smaller Larger (over 20mm)
Wall Smooth Thicker and shaggy
Cystic In early stage Not there
component
Mid line shift Usually not May
Is the MRI scan more helpful in the
differential diagnosis?
1. Contrast MRI may be able to identify smaller lesions that are
occasionally missed by CT.
2. Single REL on the CT scan might actually turn out to be multiple
lesions on the MRI.
3. RELs which have disappeared on follow up CT scans, are often
picked up on high resolution contrast MRI.
4. MRI characteristics – Tuberculomas typically demonstrate
hypointensity centrally due to caseating material. While NCC in
early stage is hyperintense.
5. MR Spectroscopy – Identifies specific biochemical
components in the granuloma. Tuberculomas typically have lipid
and lactate peaks.
6. MRI also carries the advantage of lack of radiation exposure.
MRI is also associated with certain
disadvantages
1. Calcification, often missed by MRI which is important
for differentiating between NCC and tuberculoma.
 For staging the parasitic lesions and
 Judging the effects of therapy.
2. Longer scan time, so child should be cooperative or
need to use anesthetic agents.
3. Higher cost.
Thus, CT and MRI both may need to be performed for
maximizing information yield.
If there are financial constraints, it is better to perform a CT
scan with contrast study.
One should remember that a non contrast MRI is inferior to a
contrast enhanced CT.
Are there any other tests that can help
differentiate between NCC & tuberculoma?
1. Serological tests (on blood or CSF samples)

a) Serum EITB(enzyme immunotransfer blot assay) specifity 100% ,

sesitivity 90% in >2 lesion , sensitivity 70% with single lesion

b) Hp 10 antigen assay helpful in diagnosis and follow up with treatment

with sever neurocysticercosis.

c) PCR in csf is under study.

2. Radiological scans of thigh muscles or stool examination for detecting

cysticercal disease elsewhere is usually unrewarding.

3. Finding the evidence of tuberculosis elsewhere in the body, may be

useful.
What is the place of biopsy in the
evaluation of a child with REL?

1. If there is a strong suspicion of a tumor.

2. Remains symptomatic or worsens while

on therapy,

3. If the lesion persists or increases in size

despite therapy on CT /MRI.
 Is there a role for repeating the
imaging procedure?
 When the diagnosis of the REL is uncertain,
repeating the imaging procedure after 3 months
provides clues.
 Disappearance or evolution of imaging
characteristics in REL can help diagnose NCC.

REL with edema Granular nodular stage Finally calcified stage

Neurocysticercosis
Clinical manifestations
 Usually due to cerebral oedema as a result of
intense host inflammatory response towards
dead larvae.
 Epilepsy is the most frequent symptom (50 to
80%).
 Simple or complex partial in half the cases.
 Other symptom is hemiparesis,symptom of
raised ICT (papilledema ,headach ,vomitting)
Guidelines for antiparasite treatment of
neurocysticercosis
Type Infection Recommendation evidence
burden
Parenchym Mild (1-5 Larvicidal+steriod II-3
al (cyst) cyst)
Larvicidal+steroid only if therapy related side II-3
effect
No larvicidal therapy , only radiological follow II-3
up
Moderate( Consesus: larvicidal + steroid II-3
>5 cyst)

>100 cyst larvicidal +high dose steroid III

heavy cyst
Chronic steroid treatment ,no larvicidal, III
neuroimaging follow up
Guidelines for use of anti parasite
treatment in neurocysticercosis
Type Infection Recommendation Evidence
burden
Enhancing Mild or A. Neuro imaging follow up I
lesion(degenrating moderate , no larvicidal
cyst)
B. Larvicidal with steriod II-3
C. Larvicidal , steroid only II-3
if side effect develop
Heavy Consensus No larvicidal , III
(cysticercotic high dose steroid and
encephalitis) osmotic diuretic
Calcified cysticerci Any number Consensus No larvicidal III
therapy

ctd
Guidelines for use of antiparasite
treatment in neurocysticercosis
Type Infection Recommendation Evidence
burden

Ventri cular Cosensus :Neuro endoscopic III

neurocysticercos removal when avaliable if
is not avliable then following
option
CSF diversion followed by III
anti parasite treatment

Open surgery (for mainly II-3

ventricular cyst)

Sabarachinoid Larvicidal+steroid+VP III

cyst (gaint cyst , shunt if hydrocephalous
racemose cyst)
Guidelines for use of antiparasitic
treatment in neurocysticercosis

Type Infection Recommendation Evidence

burden
Spinal (intra or Consensus: Primary III
extra medullary) surgical

Ophthalmic Consensus: Surgical II-3

cysticercosis resection of cyst
Cysticidal drugs

Drugs Dose Duration Efficacy

Praziquantel 50 mg/kg/d 15 days 60-70%

Albendazole 15mg/kg/d 28 days 75-90%

(recent
data 1 wk)
Condition where csyticidal drug is not used

1. ocular cysticercosis
2.cysticercous encephalitis
Any adverse effects of cysticidal
therapy?
 Increased seizure frequency

 Rise in ICT

Due to the host response following

destruction of parasite leading to release
of metabolic products.
Corticosteroids in NCC
 Oral prednisolone is preferred and started
2-3 days before cysticidal therapy and
continued for 7 days.
 However, high dose corticosteroids are the
primary therapy for cysticercotic
encephalitis.
 It also has role in presence of raised ICT.
Antiepileptic drugs
1. Carbamazepine, phenytoin

Duration

1) Provocative lesions : 6 months

2) Nonprovocative lesions : 2-3 years

Prognosis
1. Nearly, 85% of patients with single granuloma
have a good seizure outcome.
2. Patients with more than two seizures, and
those whose follow up CT scan shows a calcific
residue of the granuloma, have a higher risk of
recurrence and therefore epileptic drugs to be
given for longer duration.
3. The outcome of patients with multiple brain
cysts and extraparenchymal NCC depends upon
the location and severity of infestation.
What is the ultimate imaging
outcome?
 High end CT and MRI suggests lesions
often calcify but do not disappear.

 Occasionally heal with gliosis, a risk

factor for chronic epilepsy.
Tuberculomas
Incidence
Upto 40% of brain ICSOL, usually supratentorial in older and infratentorial
in younger.
Presentation
 Fever
 As slowly expending mass lesions ( ICT in 25%)
Headache, Visual or gait disturbances
 Seizures usually partial (75%)
 Focal neurological defects
Diagnosis
 Mx usually positive
 X-ray chest – evidence of pulm disease (40-50%)
 X-ray skull – calcification in 6%
 CT scan/MRI – REL
 Serology – ELISA
PCR for mycobacterium tuberculosis DNA
Treatment –
 ATT for 1 year(2 HRZE 10 HR)
 Corticosteroids for 8 to 10 week
 Prognosis – Complete disappearance in majority in
CT scan after one year.
Brain abscess
 It is focal ,suppurative infection within brain parenchyma
surrounded by vascular capsule
 Age :- any age but most common age group is 4-8yr
 Etiology:-
1. Direct spread:- eg mastoiditis ,chr ottitis media, sinusitis,
dental infection.
2. Head trauma or neuro surgical procedure
3. Hematogenous spread:- congenital heart disease with right
to left shunt eg. tetralogy of fallot.it usually lies at junction
of gray and white matter
4. cryptogenic
 Brain abscess
Stages :
 Early cerebritis:- perivascular
infilteration of inflammatory
cell,which sarround a central
core of coagulative necrosis,with
marked edema

Late cerebritis:- pus formation lead

to enlargement of necrotic centre.
Stage of late cerebritis - ill defined
capsule with large surrounding edema.
 Brain abscess
Early capsule formation:-
Formation of capsule that is CT with contrast. Note the large wall-enhancing abscess in the left
frontal lobe. The lesion is causing a shift of the brain to the right.
better developed on cortical side The patient had no neurologic signs
until just before the CT scan because the abscess is located in the
This stage correlate with frontal lobe, a “silent” area of the brain

appearance of ring enhancing

capsule on neuroimaging.

Late capsule formation:-

characterised by well defined

necrotic centre surrounded by Stage of capsule formation -
well defined ring enhancement
dense collagenous capsule .
Edema regress.
•Brain abscess
 C/F : fever , head ach ,vomiting ,focal neurological deficit depending
on location of abscess.
 Lab diagnosis:-
 CSF :-it should not be done if brain abscess suspected because it is
seldom useful and due to risk of herniation
 WBC and protein:- normal or minimally elevated
 Glucose :- normal or decreased
 CSF culture rarely positive.
 Blood culture :- positive in 10%
 Bacteriological diagnosis :- by culture of aspirated pus
 CT with contrast /MRI :- most reliable ( MRI investigation of
choice)
Brain abscess
 Treatment:-conservative management done if abscess <2cm ,short
duration illness(<2wk),no sign of ICT , child is neurologically intact
 Emperical :- vancomycin+third gen.cephalosporin
+metronidazole
 abscess after head trauma / neurosurgery :-
vancomycin +third gen. cephalosporin
 Abscess in cyanotic heart disease:-
ampicillin-sulbactam /third gen. cephalosporin
+metronidazole
 Abscess in VP shunt:- vancomycin +cefitizidime
Brain abscess
 Encapsulated causing mass effect :- treat with antibiotic and
aspiration
 Surgery is indicated if abscess is>2.5 cm , gas in abscess ,
multiloculated, located in posterior fossa , or fungus is identified

 Duration of antibiotic therapy depend on organism and response to

treatment , usually 4-6 wk .
Nocardiosis:-
mostly in immunocompromised persons, and produces poorly capsulated,
frequently multiloculated, liquefied abscesses in the brain.

Syphilitic gumma:-
may be a solitary circumscribed lesion in the brain, but this lesion
would be unusual without evidence of syphilis elsewhere.

Actinomycosis:-
invades the nervous system in 1 to 3 % patients with systemic
infection, produces a well encapsulated pus filled cavity containing
characteristic sulphur granules. Evidence of cervicofacial, thoracic or
abdominal disease is invariably present
Candida albicans:-
Immunocompromised host
multiple parenchymal brain abscess or granulomas .
Resembles tuberculoma
Candida granuloma tends to be located predominantly in white matter rather
than in the cortex
Usually associated with spinal fluid pleocytosis.
Evidence of candidiasis elsewhere in body should be present.

Acquired toxoplosmosis:-
Immunocompromised host
cicumscribed microglial nodule
hemmorragic and necrotic lesion in parenchyma
Aspergillosis:-
bronchopulmonary infection in immune compromised patients can
also result in solitary or multiple brain abscesses which progress to
form granuloma that may calcify.

Mucormycosis:-
in uncontrolled diabetic
produces intracerebral granuloma
Metastatic Tumors:-
often multiple
few appear hyperdense on CT scan
marked oedema
and mass effect on CT scan,
no calcification
evidence of primary should be present.

Primary brain tumour:- especially oligodendroglioma is likely

to calcify and produce hyperdense lesion on CAT scan
 Ring enhancing lesion on CT/MRI

Scolex
present Scolex absent

NCC Correlate clinicaly and plan for other

supportive evidence (EITB/ELISA NCC,
MONTOUX , X-ray chest , PCR /ELISA for
tuberculosis)

EITB /ELISA +VE Montoux ,x None of above +

ray,ELISA/PCR s/o think of other
NCC TB –tuberculoma causes
Message :-

CT/MRI should be correlated with

clinical finding , serological finding
and other supportive evidence of
disease for diagnosis
Bibliography
Nelson text book of pediatrics vol 1 ,18th edition
IAP test book of pediatrics 3rd edition
clinical microbiology review ,oct,p.747-756 vol .15 no 4
indian journal of tuberculosis,1996,43,45
journal of indian academy of pediatrics vol 43,march 17,2006,227-23
essential tuberculosis in children (vimlesh seth. Sk kabra)