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Cysticercosis is a common parasitic disease of the central nervous system and a pleomorphic neurological disorder. It is an endemic problem in developing countries and is now increasing in industrialised nations.1 In Mexico neurocysticercosis is one of the main reasons for neurological consultation, and the first cause of epilepsy in adults.2 The treatment of neurocysticercosis is controversial and depends on the clinical and neuroimaging features, as well as the extent and severity of the associated inflammatory reaction.3 Basal subarachnoidal cysticercosis and racemose disease of sylvian fissure may behave aggressively producing intracranial hypertension, obstructive hydrocephalus, chronic arachnoiditis, vasculitis, and cerebral infarctions.4 Subarachnoidal cysticercosis may have a chronic course and a poor prognosis, and is still treated surgically. In a recent open trial of 33 patients with subarachnoidal cysts of at least 50 mm in diameter, treatment with albendazole at a dose of 15 mg/kg/day during 28 days produced an adequate response in 12 patients (36%). The remaining 21 patients (64%) required repeated courses of albendazole and 10 treatments with praziquantel because of a partial or incomplete response to the first albendazole cycle.5 Repeated treatments are not a minor problem in areas where cysticercosis is endemic and medical resources are limited. To explore a more effective regimen for subarachnoidal cysticercosis we started a pilot study in 1998 with corticosteroids pre-treatment and a single course of a higher albendazole dose.
We included 12 patients with the diagnosis of subarachnoidal cysticercosis based in clinical data, imaging studies, and inflammatory cerebrospinal fluid with a positive enzyme linked immunosorbent assay (ELISA) test against cysticercal antigens. After written informed consent six hospitalised patients were pre-treated with intravenous dexamethasone at a dose of 8 mg every eight hours for five days. Four outpatients not receiving corticosteroids were given oral prednisone at dose of 1.5 mg/kg of body weight per day for five days. Two patients with severe arachnoiditis with incomplete response to prednisone, one of them with vasculitis proved by angiography were already receiving cyclophosphamide 100 mg per day, the drug was continued in both and one of them was also pre-treated with oral prednisone as above.
Albendazole was given at a dose of 30 mg/kg of body weight per day in three divided doses for 15 days. As soon as oral intake was tolerated patients taking dexamethasone were switched to prednisone at dose of 1 mg/kg of body weight a day. After four weeks, and depending on the clinical status prednisone dose was tapered individually. Magnetic resonance imaging (MRI) was performed before treatment and three to six months after treatment.
Four men and eight women with an average age of 32.8 years (range 20 to 47) were included. The mean hospital stay for inpatients was 17 days. Table 1 gives symptoms and signs before treatment and at the end of the 15 days of albendazole treatment. In five patients a ventriculoperitoneal shunt was placed before albendazole treatment. In seven patients, corticosteroids improved clinical manifestations within the first 24 hours.
On baseline MRI, the number of subarachnoid cysts varied from 1 to 24 cysts per patient; 10 patients had cysts in the basal cisterns and three had racemose cysts in Sylvian fissure. In three patients additional lobar and subcortical cysts were also present and ependymal or leptomeningeal enhancement was observed in five patients.
On MRI studies at six months of follow up a reduction of 86% of the number of the subarachnoidal vesicles was observed, decreasing from 73 to 10 cysts (p = 0.02; Mann-Whitney U test two tailed), with a volume reduction of 80%. Eight patients had satisfactory clinical recovery and four patients presented minor neurological deficit with functional independence.
During treatment one patient required ventriculoperitoneal shunt revision for acute intracranial hypertension. In the remaining patients the observed adverse effects were headache and nausea in two who did not required drug withdrawal.
Significant changes after treatment were observed mainly in symptoms and signs of intracranial hypertension and these were attributable to corticosteroid effects or shunting, or both. No significant modifications of glucose cells and protein levels of CSF were observed during six months of follow up. This means that chronic aracnoiditis continues after cyst destruction, and for some patients corticosteroids are necessary for long term treatment. We base our dose reductions according to clinical parameters, CSF characteristics, and leptomeningeal enhancement (MRI). In this study ELISA test’s sensitivity increased after treatment.
Pre-treatment with corticosteroids reduces the risk of complications secondary to destruction of cysticerci.4–5 In our patients an immediate clinical improvement seemed to be an indicator of adequate tolerance to subsequent albendazole treatment. Because of the variability of albendazole pharmacokinetics, we considered that treatment with 30 mg/kg/day of albendazole will increase its concentration in plasma and CSF, improving the efficacy. This small series shows that a higher albendazole dose along with corticosteroid treatment was safe and useful in the treatment of subarachnoidal cysticercosis. Patients need to be carefully selected and require close observation and to be available for long term follow up. A randomised trial of standard compared with high albendazole dose is in progress at our centre.