Neurocysticercosis
Neurocysticercosis
Prevention of neurological manifestations
Neurocysticercosis is caused by the cysticercal form, i.e. larval form of the pork tapeworm, T.solium. The larvae may locate in the brain parenchyma, intraventricular and meningeal areas, spinal canal/cord and eye, or a combination of these regions. Viable cysticerci incite little inflammatory response, but dead cysticerci elicit an increased inflammatory response.
Diagnostic criteria
Location and stage of the life cycle of the parasite in the brain determines the clinical features suspect if child from endemic area (eg. visit to Eastern Cape or pig farming area), presents with neurological abnormalities such as:
- Seizures
- Raised intracranial pressure/hydrocephalus
- Focal neurological deficits
- Cranial nerve palsies
- Meningo-encephalitis
- Meningitis
- Behavioural disorders
- Headache
Investigations
- Computed tomography (CT scan) and/or magnetic resonance imaging (MRI scan) of Brain showing cysts, peri-lesional oedema or calcification of cysts. MRI scan may identify more lesions and viable cystic lesions than the CT scan.
- Soft tissue radiology of muscles of lower limbs may demonstrate calcified cysticerci, i.e. Rice grain calcifications in muscles.
- Follow-up CT scans and/or MRI scans may help to assess the response to therapy.
Drug treatment
Calcified cysticerci and a single dying lesion visible on CT scan require no treatment or monitoring. Patients with multiple dying cysts are assumed to have active disease and require treatment. Albendazole oral 5 mg/kg/dose 8 hourly for 5 days
Prevention of neurological manifestations
In massive infestations, cysticidal therapy may trigger an inflammatory response. Delaying therapy and adding corticosteroids may lessen the risk if started < 24 hours prior to albendazole therapy. Dexamethasone IM 0.25–0.5 mg/kg/24 hours (Continue for the duration of the therapy).
OR Betamethasone oral 0.01– 0.2 mg/kg/24 hours (Continue for the duration of the therapy).