NEUROCYSTECERCOSIS DR SANDEEP BHARAT GADADE COMMAND HOSPITAL LUCKNOW.
NEUROCYSTECERCOSIS Cysticercosis - P arasitic infection that results from ingestion of eggs from the adult tapeworm, Taenia solium . Cysticercosis involves the central nervous system, it is called neurocystcerocosis. Neurocystcerocosis is acquired through consumption of food contaminated with feces of a T. solium tapeworm carrier (i.e., through fecal–oral contract ).
MODE OF INFECTION Humans are both intermediate and definitive host. Cysticercosis developed when humans are intermediate host by ingesting embryonated egg of tape worm. Release oospore penetrate gut and disseminate in body tissue. Heteroinoculolation - Egg from environment. Internal inoculation – Regurgitation from progotids into stomach. External inoculation – from infection person.
TARGET TISSUE Predilection to eye, CNS, striated muscle due to high glycogen and glucose. CNS And Eye involvement is termed as neurocystcerocosis. C /f – Manifestation and clinical features depends on location of cyst. Size of cyst, number of cyst Host immune response.
C/F SEIZURE – 70-90 % patient present with the seizure Partial onset with or without secondary generalization. Headache- indicates increased ICP or meningitis, or hydrocephalus. Nausea, vomiting Ocular Cysticercosis may present with decreased VA
PATHOGENESIS. Eggs of the tapeworm are shed in stool and contaminate food through poor hygiene. When these eggs are ingested and exposed to gastric acid in the human stomach, lose their protective capsule and turn into larval cysts, called oncospheres. Oncospheres cross the gastrointestinal tract and migrate via the vascular system to the brain, muscle, eyes, and other structures. Once in the brain, the larval cysts (cysticerci) initially generate a minimal immune response and may remain in the brain as viable cysts for years.
Life cycle of TINEA
stages of cysts within the parenchyma of the brain Vesicular : Magnetic resonance imaging (MRI) of a vesicular cyst. Note the well-defined scolex, minimal contrast enhancement, and mass effect. Colloidal -MRI of a colloidal cyst. Note ring enhancement, loss of the scolex, and perilesional edema . N odular/granular stage - Note nodule with diffuse enhancement and no cystic component . Calcified granuloma- Noncontrast computed tomography showing multiple punctuate calcifications.
INVESTIGATION Stool routine And microscopy. Fundoscopy Biopsy & Histopathology. CT with contrast, MRI ELISA CSF - Detection of anticysticercal antibodies in the CSF by ELISA is 89% sensitive and 93% specific in patients with viable neurocystcerocosis infections. E nzyme-linked immunoelectrotransfer blot (EITB) assay - Uses lentil lectin purified glycoprotein antigens (LLGP) to detect antibodies to T solium in serum. EITB sensitivity is around 98% for patients with two or more live parasites in the nervous system.
Treatment Treatment may changes with location of involvement Intraparenchymal – calcified lesion or viable degenerative lesion. Extraparenchymal- intraventricular involvement or subarachnoid.
Albendazole and praziquantel are the principal ant parasitic drugs used to treat neurocystcerocosis. Antiparasitic drugs praziquantel and albendazole reduce the number of cysts and frequency of seizures. Albendazole 15mg/kg/day – fatty meal improves absorption 7 days for single parenchymal lesions. Longer duration and higher doses ( upto 30mg/kg/day) or combination with praziquantel for multiple lesions or subarachnoid involvement.
+ Recent trials Showed improved resolution with combination therapy of Albendazole, praziquantel and corticosteroids. Praziquantel 50-100mg/kg/day Divided doses daily for 28 days can be used in combination with Albendazole or alternative to it. Patient should be medicated with prednisolone 1-2mg/kg/day or oral dexamethasone 0.15mg/kg/day before starting antiparsititc drug . Methotrexexate can be used alternative to steroids as steroids sparing agent in prolong anti-inflammatory therapy.