Date Published: April 04, 2018
Publisher: The American Society of Tropical Medicine and Hygiene
Author(s): A. Clinton White, Christina M. Coyle, Vedantam Rajshekhar, Gagandeep Singh, W. Allen Hauser, Aaron Mohanty, Hector H. Garcia, Theodore E. Nash.
Guidelines for the clinical management of patients with neurocysticercosis (NCC) were prepared by a panel of the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH). The guidelines are intended for infectious disease specialists, neurologists, neurological surgeons, internists, pediatricians, and family practitioners.
In the first section, the panel summarizes background information relevant to the topic. In the second section, the panel poses questions regarding the diagnosis and treatment of NCC, evaluates applicable clinical trial and observational data, and makes recommendations using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework.1 The following 27 clinical questions were answered:I.How should NCC be diagnosed?II.What imaging studies should be used to classify disease?III.What additional tests should be performed before initiation of therapy?IV.How should antiparasitic and anti-inflammatory therapy be monitored?V.What is the role of antiparasitic drugs in VPN?VI.What is the role of anti-inflammatory therapy in management of VPN?VII.What is the role of antiepileptic drugs in VPN?VIII.What follow-up is recommended after initial antiparasitic therapy for patients with VPN?IX.What should be the initial approach to the patient with multiple enhancing lesions from NCC?X.What is the role of antiepileptic medications in patients with SEL from cysticercosis with seizures?XI.What is the role of antiparasitic drugs in patients with SEL?XII.What is the role of anti-inflammatory therapy in SEL?XIII.How should patients with SEL be followed?XIV.What should the initial approach be to patients with calcified lesions suggestive of CPN?XV.What is the role of antiparasitic drugs, antiepileptic drugs, and anti-inflammatory medications in the management of patients with CPN?XVI.Is there a role for surgical therapy in refractory cases?XVII.How are extra parenchymal cysts best identified?XVIII.What is the optimal approach to management of IVN in the lateral and third ventricles?XIX.What is the optimal surgical approach to management of IVN in the fourth ventricles?XX.What is the optimal approach to adherent IVN?XXI.Does medical therapy as an adjunct to procedures or as primary therapy have an impact on outcome in treating patients with IVN?XXII.What is the role of medical therapy in SAN in the basilar cisterns or Sylvian fissures?XXIII.What is the role of neurosurgery in SAN?XXIV.How is SN best treated?XXV.What is the optimal management of OC?XXVI.Should children be managed differently from adults?XXVII.Should management be different in pregnant women?
NCC, caused by the larval form of the cestode parasite Taenia solium, is a major cause of seizure and neurologic disease worldwide and is common among immigrant populations in the United States. Highly endemic regions include Latin America, sub-Saharan Africa, and parts of Asia.2,3 In endemic areas, it is linked to approximately 29% of cases of seizures.4 Estimates suggest that there are more than 2,000 cases per year in the United States with hospital charges of nearly $100 million per year.5,6 Humans can be hosts to both the tapeworm form and larval forms of the parasite. Taeniasis (also termed taeniosis) refers to infestation of the human intestines with the tapeworm form. The tapeworm is acquired by ingestion of undercooked pork. The scolex evaginates and attaches to the intestinal wall and segments termed proglottids form a long ribbon-like chain referred to as the strobili. The gravid proglottids and eggs are passed in stool. Humans can also develop cysticercosis after ingestion of ova. Cysticercosis refers to infection of the tissues with the larval cyst (or metacestode). Normally, pigs host the cysts, which are acquired by ingestion of ova or proglottids from human feces. However, humans can be infected by ingestion of ova and develop cysticercosis. Neurocysticercosis refers to cysticercosis involving the central nervous system, including the brain parenchyma, ventricles, basilar cisterns, sulci, gyri, spine, and retina.
More than 2,000 cases of NCC are diagnosed each year in the United States.5,6 Epidemiologic studies suggest that NCC is the cause of approximately 29% of seizures in endemic areas and about 2% of patients presenting with seizures presenting to U.S. emergency rooms.2–5,8–10 The seizures can be focal, focal with generalization, or generalized. Thus, NCC should be considered in all patients with seizures potentially exposed to a tapeworm carrier. Increased intracranial pressure is also a common manifestation of NCC. Approximately 20% of cases present with increased intracranial pressure, mainly obstructive hydrocephalus.2–4,8,10,11