Clinical and Immunologic Follow-up Study of Patients with Neurocysticercosis After Treatment with Praziquantel

Abstract

Article abstract-In a prospective study, 17 Brazilian patients with parenchymatous neurocysticercosis were monitored for a period of 12 months after treatment with praziquantel. Taenia solium-specific IgG antibodies, interleukin-1beta (IL-1beta), tumor necrosis factor alpha, neopterin, and soluble interleukin-2 receptor (sIL-2R) were measured in serum and CSF before starting the therapy, on the last day of treatment, 5 weeks after treatment, and 3, 6, and 12 months after treatment. The most common symptoms and signs found in patients before treatment were headache, neck stiffness, and seizures. Six months after commencement of therapy, 13 of the 17 patients were free of complaints. Clinical normalization was paralleled by a significant decrease (p < 0.05) in the amount of intrathecally produced anti-T solium IgG 1 year after treatment. IL-1beta was undetectable in serum at all times, whereas in the CSF it was within the normal range during the whole study period. The mean concentration of sIL-2R in the CSF was 65 kU/l (normal, <50 kU/l) 5 weeks after treatment, whereas in all subsequent investigations sIL-2R was undetectable. The median CSF neopterin level was slightly elevated before treatment (6.8 nmol/l). One year after treatment, it had dropped by 69% (p < 0.001) to a median value of 2.1 nmol/l. The size of planimetrically measured focal cystic brain lesions on CT correlated with the amount of intrathecally synthesized anti-T solium IgG at the end of the study (r = 0.89, p < 0.05). The intrathecal patterns of specific anti-T solium IgG, IL-1beta, sIL-2R, and neopterin indicate that the main immune response in neurocysticercosis is predominantly intrathecal, involving humoral as well as cell-mediated mechanisms. Neuroimmunologic effects in the course of the disease seem to be of a long-term nature since some of the markers (intrathecally produced anti-T solium IgG and neopterin in the CSF) normalize after successful drug therapy lasting a minimum of 6 months.NEUROLOGY 1995;45: 532-538