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History
A 58 years old- male patient with chief complaint incoherent speech with behavorialdisorder
and also memory loss since 5 days ago. He had a habbit of recreational boar hunting in forest and
ate undercooked pork during his hunting sessions. He had a history of non-hemorrhagic stroke
on October 2017 along with hypertension and type II diabetes mellitus with sequele of left slight
hemiparese. In November 2017, diagnosed with non-hemorrhagic stroke, manifested in focal
seizure.
Relevant Laboratory
Hb 10,9 g/dL
WBC 15.400 uL
Platelet 350.000 uL
CRP 93,5 mg/l
Cysticercosis antibody (ELISA) Positive
Ureum 58 mg/dL
Creatinin 2,3 mg/dL
Imaging Studies
MRI of the brain without contrast because of high level of blood creatinin.
On T2FSE shows multiple cysts subcentimeter hyperintens lesions with hypointens “dot”
inside it at the area of bilateral cerebellum, left pons, right dorsal mescencephalon, cortical, and
bilateral subcortical temporoocipital, bilateral frontal, bilateral parietal, bilateral base of ganglia,
bilateral thalamus, bilateral body of callosum, bilateral corona radiata, and bilateral semiovale
centrum,
with T1 SE shows hypointense cysts with centric and eccentric hyperintense area inside of it.
On T2 Fat Sat Dark Fluid shows perifocal edema on most of the lesions.
On SWI, some lesions show dark signal focal.
DISCUSSION
After the cysticerci reach the brain, the first is the vesicular stage characterized by a cyst with a
translucent vesicular wall, transparent fluid, and a viable invaginated scolex, may remain in this
stage for years or degenerate. The cyst then develops a thick vesicular wall, the fluid becomes
turbid, and the scolex degenerates during the next stage, which is termed the colloidal stage. In
granular nodular stage, cyst wall thickens and scolex is mineralized granule. Lession becomes
completely mineralized and small in nodular calcified stage.
There are diagnostic criteria for neurocysticercosis. Definitive diagnosis with the presence one of
absolute criteria : histological demonstration of parasite from the biopsy or evidence of cystic
lession showing scolex on neuroimaging studies or direct visualization of subretinal parasites by
funduscopy.
After the cysticerci reach the brain, the first is the vesicular stage : viable invaginated scolex,
may remain for years or degenerate. The scolex degenerates during next stage: the colloidal
stage. Then in granular nodular stage: scolex mineralized granule. Then it becomes completely
mineralized and small in nodular calcified stage.
Absolute
- Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion
Major
Minor
Definitive
- Presence of two major plus one minor and one epidemiological criteria
Probable
- Presence of one major plus one minor and one epidemiological criteria
Absolute criteria include: histological confirmation of parasites, evidence of subretinal cysts, and
demonstration of the scolex within a cyst.
Neuroimaging criteria are categorized as major (cystic lesions without scolex, enhancing lesions,
multilobulated cysts, and calcifications), confirmative (resolution of cysts after cysticidal drug
therapy, spontaneous resolution of single enhancing lesions, and migrating ventricular cysts on
sequential neuroimaging studies) and minor (hydrocephalus and leptomeningeal enhancement).
REFERENCES
1. Del Brutto OH,et al. Revised Diagnostic Criteria for Neurocysticercosis. J Neurol Sci.
2017 Jan 15; 372:202-210.
2. Sahu PS, et al. Imaging and Serological-Evidence of Neurocysticercosis among Patients
with Seizure in Odisha, an Unexplored Eastern Coastal Province in India.Journal of
Clinical and Diagnostic Research. May2015;Vol 9(5);6-10
3. DeGiorgio CM, et al. Epilepsy current : Current Review Neurocysticercosis. Vol4.No.3.
June 2004 ; 107-111.
4. Widarso HL, et al. Prevalensi dan Distribusi Taeniasis dan Sistiserkosis. 2001. Makara
Kesehatan.Vol5 :34-38.
BACKGROUND:
A unified set of criteria for neurocysticercosis (NCC) has helped to standardize its diagnosis in different settings.
METHODS:
Cysticercosis experts were convened to update current diagnostic criteria for NCC according to two principles: neuroimaging
studies are essential for diagnosis, and all other information provides indirect evidence favoring the diagnosis. Recent
This revised set is structured in absolute, neuroimaging and clinical/exposure criteria. Absolute criteria include: histological
confirmation of parasites, evidence of subretinal cysts, and demonstration of the scolex within a cyst. Neuroimaging criteria
are categorized as major (cystic lesions without scolex, enhancing lesions, multilobulated cysts, and calcifications),
confirmative (resolution of cysts after cysticidal drug therapy, spontaneous resolution of single enhancing lesions, and
migrating ventricular cysts on sequential neuroimaging studies) and minor (hydrocephalus and leptomeningeal
enhancement). Clinical/exposure criteria include: detection of anticysticercal antibodies or cysticercal antigens by well-
standardized tests, systemic cysticercosis, evidence of a household Taenia carrier, suggestive clinical manifestations, and
residency in endemic areas. Besides patients having absolute criteria, definitive diagnosis can be made in those having two
major neuroimaging criteria (or one major plus one confirmative criteria) plus exposure. For patients presenting with one
major and one minor neuroimaging criteria plus exposure, definitive diagnosis of NCC requires the exclusion of confounding
pathologies. Probable diagnosis is reserved for individuals presenting with one neuroimaging criteria plus strong evidence of
exposure.
CONCLUSIONS:
This revised set of diagnostic criteria provides simpler definitions and may facilitate its more uniform and widespread