This action might not be possible to undo. Are you sure you want to continue?
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
Neurocysticercosis (NCC) Tuberculoma Brain abscess Toxoplasmosis Fungal granuloma Syphilitic gumma Nocardia Actinomycosis Cryptococcus neoformans Candida Albicans Aspergillosis Mucoromycosis Lymphoma Glioma Metastasis Demyelinating plaques
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.
Mode of infestation
Contaminated food or water with eggs of pork tapeworm
Oncospheres in Gut (Primary larvae) Intestinal mucosa Circulatory system Brain Muscle
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 parasite from biopsy of brain. of the
Cystic lesions with scolex on CT or MRI
Direct visualization of 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 infection. Individual coming from living in an endemic area, History of travel to an endemic area. solium
Diagnosis of neurocysticercosis
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 areNCC Location Parietal (subcortical interface), temporal, Frontal, Occipital Single or more Smaller Smooth In early stage Usually not TUBERCULOMA Basal regions in posterior fossa in younger children Often multiple, satellite lesion Larger (over 20mm) Thicker and shaggy Not there May
Number Size Wall Cystic component Mid line shift
Is the MRI scan more helpful in the differential diagnosis?
1. 2. 3. 4. Contrast MRI may be able to identify smaller lesions that are occasionally missed by CT. Single REL on the CT scan might actually turn out to be multiple lesions on the MRI. RELs which have disappeared on follow up CT scans, are often picked up on high resolution contrast MRI. MRI characteristics – Tuberculomas typically demonstrate hypointensity centrally due to caseating material. While NCC in early stage is hyperintense.
– Identifies specific biochemical components in the granuloma. Tuberculomas typically have lipid and lactate peaks. MRI also carries the advantage of lack of radiation exposure.
MRI is also associated 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)
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
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 raised ICT (papilledema ,headach ,vomitting) of
Guidelines for antiparasite treatment of neurocysticercosis
Type Parenchym al (cyst) Infection burden Mild (1-5 cyst) Recommendation Larvicidal+steriod Larvicidal+steroid only if therapy related side effect No larvicidal therapy , only radiological follow up Moderate( Consesus: larvicidal + steroid >5 cyst) >100 cyst heavy cyst larvicidal +high dose steroid Chronic steroid treatment ,no larvicidal, neuroimaging follow up evidence II-3 II-3 II-3 II-3
Guidelines for use of anti parasite treatment in neurocysticercosis
Type Infection burden Recommendation Evidence Enhancing Mild or lesion(degenrating moderate cyst) A. Neuro imaging follow up I , no larvicidal B. Larvicidal with steriod C. Larvicidal , steroid only if side effect develop Heavy (cysticercotic encephalitis) Calcified cysticerci Any number Consensus No larvicidal , high dose steroid and osmotic diuretic Consensus No larvicidal therapy II-3 II-3 III
Guidelines for use of antiparasite treatment in neurocysticercosis
Type Infection burden Recommendation Evidence Ventri cular neurocysticercos is Cosensus :Neuro endoscopic III removal when avaliable if not avliable then following option CSF diversion followed by anti parasite treatment Open surgery (for mainly ventricular cyst) Sabarachinoid cyst (gaint cyst , racemose cyst) Larvicidal+steroid+VP shunt if hydrocephalous III
Guidelines for use of antiparasitic treatment in neurocysticercosis
Spinal (intra or extra medullary) Ophthalmic cysticercosis
Consensus: Primary surgical Consensus: Surgical resection of cyst
Drugs Dose Duration Efficacy
Praziquantel 50 mg/kg/d 15 days
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.
1. Carbamazepine, phenytoin Duration 1) Provocative lesions : 6 months 2) Nonprovocative lesions : 2-3 years
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.
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.
It is focal ,suppurative infection within brain parenchyma 1.
surrounded by vascular capsule Age :- any age but most common age group is 4-8yr Etiology:Direct spread:- eg mastoiditis ,chr ottitis media, sinusitis, dental infection. Head trauma or neuro surgical procedure Hematogenous spread:- congenital heart disease with right to left shunt eg. tetralogy of fallot.it usually lies at junction of gray and white matter cryptogenic
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.
Early capsule formation:Formation of capsule that is better developed on cortical side This stage correlate with appearance of ring enhancing capsule on neuroimaging.
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. The patient had no neurologic signs until just before the CT scan because the abscess is located in the frontal lobe, a “silent” area of the brain
Late capsule formation:-
characterised by well defined necrotic centre surrounded by dense collagenous capsule . Edema regress.
Stage of capsule formation well defined ring enhancement
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)
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
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 .
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
Correlate clinicaly and plan for other supportive evidence (EITB/ELISA NCC, MONTOUX , X-ray chest , PCR /ELISA for tuberculosis)
EITB /ELISA +VE NCC
Montoux ,x ray,ELISA/PCR s/o TB –tuberculoma
None of above + think of other 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)