Abstract

.Subarachnoid neurocysticercosis (SUBNCC) is usually caused by an aberrant proliferative form of Taenia solium causing mass effect and arachnoiditis. Thirty of 34 SUBNCC patients were treated with extended cysticidal and anti-inflammatory regimens and followed up a median of 4.2 years posttreatment (range: 15 for ≥ 4 years, 20 ≥ 2 years, 26 > 1 year, and 3 < 1 year). The median ages at the time of first symptom, diagnosis, and enrollment were 29.7, 35.6, and 37.9 years, respectively; 58.8% were male and 82.4% were Hispanic. The median time from immigration to symptoms (minimum incubation) was 10 years and the estimated true incubation period considerably greater. Fifty percent also had other forms of NCC. Common complications were hydrocephalus (56%), shunt placement (41%), infarcts (18%), and symptomatic spinal disease (15%). Thirty patients (88.2%) required prolonged treatment with albendazole (88.2%, median 0.55 year) and/or praziquantel (61.8%; median 0.96 year), corticosteroids (88.2%, median 1.09 years), methotrexate (50%, median 1.37 years), and etanercept (34.2%, median 0.81 year), which led to sustained inactive disease in 29/30 (96.7%) patients. Three were treated successfully for recurrences and one has continuing infection. Normalization of cerebral spinal fluid parameters and cestode antigen levels guided treatment decisions. All 15 patients with undetectable cestode antigen values have sustained inactive disease. There were no deaths and moderate morbidity posttreatment. Corticosteroid-related side effects were common, avascular necrosis of joints being the most serious (8/33, 24.2%). Prolonged cysticidal treatment and effective control of inflammation led to good clinical outcomes and sustained inactive disease which is likely curative.

Highlights

  • Neurocysticercosis (NCC) is caused by infection of the brain with metacestodes or cysts of the pork tapeworm, Taenia solium

  • Prolonged cysticidal treatment and effective control of inflammation led to good clinical outcomes and sustained inactive disease which is likely curative

  • Consideration to stop therapy occurred when MRI imaging was improved with moderation and stabilization of enhancement, decreased or serial decreases in cestode antigen concentrations to low or undetectable levels, successive decrease in cerebral spinal fluid (CSF) white blood cell counts (WBCs) counts, and improved or stable clinical state of the patient

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Summary

INTRODUCTION

Neurocysticercosis (NCC) is caused by infection of the brain with metacestodes or cysts of the pork tapeworm, Taenia solium. Infection of the brain parenchyma, ventricles, and subarachnoid space typically causes distinctive clinical manifestations. In its most advanced form, multiple brain cisterns are enlarged causing varying degrees of mass effects. Inflammation (manifested as enhancement on MRI) is usually limited[6,13] but with progression or cysticidal treatment, acute and chronic arachnoiditis ensues directed toward degenerating cysts and residual antigen.[6] Long-standing Inflammation is responsible for many of the severe and often fatal complications of SUBNCC, including hydrocephalus, focal brain damage, nerve entrapments, and infarcts.[2,7] There are no randomized treatment trials and no studies to determine effectiveness and best use of cysticidal drugs, corticosteroids, duration of treatment, or the utility of other immunosuppressive medications. Intensity and duration of treatments, guided by improvement in CSF parameters and cestode antigen levels, resulted in no mortality, good clinical outcome, and sustained inactive disease in all but one patient

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