Draft Neurocysticercosis.docx

Introduction Neurocysticercosis (NCC) is a neurologic infection caused by the larval stage of the tapeworm Taeniasolium. In the developing countries, the infection of the central nervous system (CNS) due to the Taeniasolium larvae, is the most common cause of acquired epilepsy. The prevalences of taeniasis/cysticercosis in Indonesia were between 1-42.7%, mostly found in three provinces : North Sumatra, Bali, and Irian Jaya. The adult tapeworm develops in human hosts after they ingest live cysticercus in undercooked pork.Pigs become infected by eggs or gravid proglotids, invade intestinal wall and migrated to striated muscle, where they develop into cysticerci. NCC develops when humans accidentally ingest eggs. Adult tapeworms shed proglottids, and each proglottid contains approximately 1000 to 2000 eggs. Once the hexacanth embryo reaches the parenchyma it forms cysticerci which undergo four stages of involution. The first is the vesicular stage characterized by a cyst with a translucent vesicular wall, transparent fluid, and a viable invaginatedscolex, 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.

Eggs or gravid proglottids are passed with feces

; the eggs can survive for days to months in the environment. Cattle (T.

saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids

. In

the animal's intestine, the oncosphereshatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat

. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm,

which can survive for years. The adult tapeworms attach to the small intestine by their scolex

and reside in the small

intestine . Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T. saginataadults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively.

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 WBC Platelet CRP Cysticercosis antibody (ELISA) Ureum Creatinin

10,9 g/dL 15.400 uL 350.000 uL 93,5 mg/l Positive 58 mg/dL 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. Definitive diagnosis criteria 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. Presence of two major : evidence of highly suggestive of ncc in neuroimaging studies, positive serum immunoblot of anticysticercal antibodies, resolution of intracranial cystic lession after therapy with albendazole, spontaneus resolution of small single enhancing lesion.

Absolute - Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion - Evidence of cystic lesions showing the scolex on neuroimaging studies - Direct visualization of subretinal parasites by fundoscopic examination Major - Evidence of lesions highly suggestive of neurocysticercosis on neuroimaging studies

- Positive serum immunoblot for the detection of anticysticercal antibodies - Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel - Spontaneous resolution of small single enhancing lesions Minor - Evidence of lesions compatible with neurocysticercosis on neuroimaging studies - Presence of clinical manifestations suggestive of neurocysticercosis - Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens - Evidence of cysticercosis outside the central nervous system Epidemiological - Individuals coming from or living in an area where cysticercosis is endemic - History of travel to disease-endemic areas - Evidence of a household contact with T. solium infection Degrees of diagnostic certainty Definitive - Presence of one absolute criterion - Presence of two major plus one minor and one epidemiological criteria Probable - Presence of one major plus two minor criteria - Presence of one major plus one minor and one epidemiological criteria - Presence of three minor plus 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). 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. REFERENCES 1.

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Del Brutto OH,et al. Revised Diagnostic Criteria for Neurocysticercosis. J Neurol Sci. 2017 Jan 15; 372:202-210. 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 DeGiorgio CM, et al. Epilepsy current : Current Review Neurocysticercosis. Vol4.No.3. June 2004 ; 107-111. Widarso HL, et al. Prevalensi dan Distribusi Taeniasis dan Sistiserkosis. 2001. Makara Kesehatan.Vol5 :34-38.

a definitive diagnosis of NCC cannot be established without the aid of neuroimaging.

CNS Imaging in Cysticercosis 

Updated: Nov 12, 2015 Author: Anil Khosla, MBBS, MD;

Revised diagnostic criteria for neurocysticercosis J Neurol Sci. 2017 Jan 15;372:202-210. doi: 10.1016/j.jns.2016.11.045. Epub 2016 Nov 21.

Revised diagnostic criteria for neurocysticercosis. Del Brutto OH1, Nash TE2, White AC Jr3, Rajshekhar V4, Wilkins PP5, Singh G6, Vasquez CM7, Salgado P8, Gilman RH9, Garcia HH10. Author information Abstract 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 diagnostic advances were incorporated to this revised set.

RESULTS:

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 wellstandardized 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 applicability in different scenarios.