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By Michele Barry, MD, FACP
Dr. Robert Gilman convened an important symposium on neurocysticercosis (NCC) at the annual meeting of the American Society of Tropical Medicine and Hygiene. During that symposium, Dr. Theodore Nash from NIAID reported on the increasing evidence indicating that calcific neurocysticercosis is not necessarily clinically inactive, but may be a cause of seizures and focal symptoms associated with episodic perilesional edema. It is well known that seizures may be common when viable or degenerating cysts are present. In contrast, few if any symptoms have been attributed previously to chronic calcific cysticercosis. Dr. Nash presented the case of a 48-year-old woman, born in the United States, who was referred to the NIH for cysticerosis contracted in India and found to be refractory to medical therapy. She was treated in 1986 when she had fever, multifocal seizures, and positive serology. By 1987, no cystic lesions remained, but 55 residual calcified cysticerci were scattered in her brain parenchyma. She then presented with episodic epilepsy and neurologic symptoms over many years, always precipitating full antiparasitic drug therapy along with corticosteroids. Each relapse was associated with perilesional edema appearing as a bright signal using MRI flair or T2 imaging.
Dr. Nash postulated several potential mechanisms. They included direct injury to brain tissue associated with single calcified granulomas. Such lesions could cause gliosis around foci and be associated with seizure activity. Also, some of the calcified lesions may have contained a scolex, as has been reported previously. These could periodically release parasitic antigens resulting in perilesional edema. Another hypothesis was calcium toxicity as a possible cause of seizures. Calcium might form an insoluble matrix that could release incorporated antigens on occasion. Corticosteroids and multiple anticysticidal courses of therapy were used in treating his patient with relapsing perilesional edema (see Suggested Reading).
In a separate presentation by Dr. Hector Garcia of Universidad Peruana Cayetano Heredia in Lima, Peru, more data were presented to resolve the issue as to whether antiparasitic drugs are necessary for acute NCC with 20 or fewer cystic lesions. They conducted a double-blind, randomized trial in 120 patients with seizures due to parenchymal NCC with 20 or fewer cysts. All patients were given standard anti-epileptic treatment and randomized to treatment with albendazole 400 b.i.d. for 10 days and dexamethasone 0.1 mg/kg/d for 10 days or double placebo for 10 days. Patients were evaluated by MRI scanning at 6 months and CT scans done 12 and 24 months after treatment. Clinical evaluations were performed at day 15 and 30 and every 3 months for 2 years or for 1 seizure-free year after withdrawal of anti-epileptic drugs. While the overall numbers of patients with 1 seizure were the same for both groups, the frequency of grand mal seizures was significantly lower (65%) in the treatment group. At 6 months, the placebo group had 87% viable cysts by CT scan and, surprisingly, the albendazole/dexamethasone group had 41% viable cysts by CT criteria. They concluded that antiparasitic drugs are the treatment of choice for this type of NCC.1
Comment by Michele Barry, MD, FACP
Finally, there has been some resolution of the question about treating low-burden NCC or single parenchymal cysts. Clearly, the treatment group in the data presented by Garcia showed fewer grand mal seizures after treatment.1 In an accompanying editorial, Dr. James Maguire points out that more patients in the albendazole group had seizures during treatment, as would be expected, but by 2 months this trend reversed and the placebo group had more generalized and more frequent seizures for the rest of the 18-month follow-up.2 What is curious about the results of therapy was the strikingly poor success rate for the eradication of viable cysts using a 10-day course of albendazole (40% viable cysts persisted). This is surprising given that an 8-day course of albendazole has been shown to be equivalent to a 15-day course in other studies. Perhaps MRI follow-up is a more sensitive way to demonstrate cyst viability? Perhaps we should be treating with longer course therapy?
Dr. Nash’s presentation of the apparently relapsing symptoms of NCC, correlating with perilesional edema around appropriately treated calcified lesions over many years, implies some possible episodic immunologic reactions to parasitic antigen in old, calcified granulomas among other explanations. Regardless of the explanation, attention must be paid. Leutscher and Andriantsimahavandy reported on their evaluation of 73 Peace Corps volunteers who had been stationed in Madagascar, where cysticercosis is endemic.3 Six (8.2%) were found to be seropositive; 1 demonstrated 2 intraparenchymal noncalcified cysts in the frontal lobe requiring therapy. Screening asymptomatic people who have immigrated from, or been long-term residents within, endemic areas for cysticercosis calls for increased consideration of screening and therapy based upon these findings.
Dr. Barry, Professor of Medicine; Co-Director, Tropical Medicine and International Travelers’ Clinic, Yale University School of Medicine, is Associate Editor of Travel Medicine Advisor.
1. Garcia HH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. 2004;350:249-258.
2. Maguire JH. Tapeworms and seizures—Treatment and prevention. N Engl J Med. 2004;350:215-217.
3. Leutscher P, Andriantsimahavandy A. Cysticercosis in Peace Corps volunteers in Madagascar. N Engl J Med. 2004;350:311-312.
1. Nash T, et al. Cerebral calcified cysticercosis and epileptogenesis. Neurology. 2004. In press.
2. Nash T, et al. Calcified cysticerci provoke perilesional edema and seizures. Clin Infect Dis. 2001;33:1649-1653.