Neuroimaging in Neurocysticercosis Treatment & Management
- Author: Arturo Carpio, MD; Chief Editor: Niranjan N Singh, MD, DM more...
Because of the variable clinical course of neurocysticercosis (NC), treatment must be individualized for each patient.
Symptomatic treatment (see the image below) includes corticosteroids for intracranial edema and inflammation, antiepileptic drugs for secondary acquired epilepsy, analgesic medication for headache, and osmotic agents such as mannitol or glycerol for intracranial hypertension.
First seizures due to inflamed cysticercal lesions should be considered acute symptomatic seizures. Therefore, they should be treated only for the duration of the acute condition. However, treatment may be continued during the period when the inflammatory response is active, which might last several months.
No guidelines exist for the time for which antiepileptic drugs (AED) should be continued following an acute neurocysticercosis episode. The risk of seizures is substantial as long as an active ongoing process, as characterized by persistence of edema around the degenerating lesion, is present. Because of this risk, CT scans are useful for treatment decisions.
Seizures in the context of edema and a degenerative lesion should be considered acute symptomatic seizures, even if they occur many months after presentation. After resolution of the acute lesion, AED administration may be discontinued.
Seizures occurring after resolution of edema or calcification of the degenerating cyst should be considered unprovoked, and, in this situation, long-term AED administration is warranted (see the image below). Other authors also suggest that AED administration can be safely withdrawn once the follow-up CT scan shows resolution of the lesion.
Clinical controversy has centered on the role of cysticidal agents for the treatment of symptomatic NC. Cysticidal agents in current use for NC include praziquantel and albendazole.[8, 9] Cysticidal therapy may hasten radiologic resolution of cysts but can be associated with exacerbation of neurologic symptoms; the possibility exists of massive cerebral edema and death in some individuals who have multiple cysts.
Some authors have advocated simultaneous administration of steroids to reduce the inflammatory response and exacerbation of symptoms, but the safety of this treatment has not been evaluated fully. In developing countries, most neurologists administer the steroids and cysticidal drugs at the same time.
Patients with NC are possibly more likely to remain seizure-free if cysticidal treatment is administered; however, recent studies have shown that there is no correlation between treatment with cysticidal drugs and seizure recurrence.
A meta-analysis of randomized trials assessing the effect of cysticidal drugs (albendazole and praziquantel) on neuroimaging and clinical outcomes of patients with NC has been reported. The search identified 764 papers, of which only 11 met the inclusion criteria, from which 5 were qualified as “good quality.” Among these 5 studies, just 2 were carried out on patients with active or viable cysts, and the remaining 3 studies were performed on transitional or degenerative cysts, in which the parasite is already dead and therefore the treatment with cysticidal drugs is probably worthless. The effects of treatment on neuroimaging end points were relatively small (odds ratios > 2.2). The editors of this paper concluded that the 11 selected studies were small and heterogeneous and provided limited evidence of a modest effect of cysticidal treatment in patients with NC.
During the last few years, 2 double-blind, randomized, placebo-controlled trials to evaluate the effects of cysticidal treatment (albendazole) in patients with NC have been published. Garcia et al concluded that antiparasitic therapy in patients with viable parenchymal cysts is safe and effective; however, 6 months after treatment, only 38% of patients had cysts that disappeared on neuroimaging in comparison with 15% of patients who used placebo. Carpio et al reported disappearance of cysts in 35% of patients with viable cysts in comparison with 12% of the placebo group. In both studies, these differences were statistically significant (p < 0.05).
Based on these 2 studies, cysticidal treatment using albendazole is effective in terms of disappearance of viable parenchymal cysts in one third of patients.
The study of Carpio et al found a reduction in the number of active extraparenchymal cysts (intraventricular and subarachnoideal) in the albendazole group compared with the placebo group, although it was not statistically significant.
No definitive data exist pertaining to combination antihelminthic therapy or whether the use of steroids increases or decreases antihelminthic dosage requirements.
Surgical treatment should be restricted to removal of the parasite located in the subarachnoid (racemose form) or ventricular area, and to ventriculoperitoneal shunting for the treatment of decompensated hydrocephalus (see the image below).
Surgery should not be considered for parenchymal cysts without regard to location, size, or stage of evolution, because this form of NC can be controlled only by symptomatic treatment (or presumably by etiologic treatment). In addition, surgical sequelae could result in more brain damage than the parasite itself.
Transitional or degenerative cysts, regardless of their size or location (see the images below), should not be biopsied or removed since the parasite is dead and will disappear or be calcified spontaneously.
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