A revision of literature was done with the objective of tracing an epidemiologic profile of neurocysticercosis (NCC) in Brazil. The prevalence was 0.12-9% in autopsies. The frequency was 0.03-7.5% in clinical series and 0.68-5.2% in seroepidemiological studies. The disease corresponds to 0.08-2.5% of admissions to general hospitals. Patient origin was rural in 30-63% of cases. The most involved age range (64-100%) was 11 to 60 years, with a predominance (22-67%) between 21 and 40 years. The male sex was the most affected (51-80%). In the severe forms there was a predominance of urban origin (53-62%) and of the female sex (53-75%). The period of hospitalization ranges from 1 to 254 days and 33 to 50% of patients suffer 1.7 ± 1.4 admissions. The clinical picture was variable, with a predominance of epileptic syndrome (22-92%) and intracranial hypertension (19-89%). Psychiatric manifestations were associated in 9-23% of patients. Lethality was 0.29% in terms of all diseases in general and 4.8-25.9% in terms of neurologic diseases. The asymptomatic form was detected in 6% of patients in clinical serie and in 48.5% of case from autopsies. The racemose form and ventricular localization also was observed as asymptomatic form. Among the patients with cutaneous cysticercosis 65% of them showed neurologic manifestations.

RESUMO -Com o objetivo de mostrar as características da neurocisticercose (NCC) no Brasil, realizou-se análise critica da literatura nacional que mostrou incidência de 1,5% nas necropsias e de 3,0% nos estudos clínicos, correspondendo a 0,3% das admissões em hospitais gerais. Em estudos soroepidemiológicos, a positividade para cisticercose foi de 2,3%. O paciente brasileiro com NCC pode apresentar um perfil clínico-epidemiológico geral (homem, 31-50 anos, procedência rural, manifestações epilépticas parciais complexas, LCR normal ou hiperproteinorraquia, calcificações ao exame de TC, constituindo a expressão da forma inativa da NCC) e outro de gravidade (mulher, 21-40 anos, procedência urbana, manifestações de cefaléia vascular e HIC, típica síndrome do LCR ou alteração de dois ou mais parâmetros, vesículas associadas ou não a calcificações ao exame de TC, constituindo a expressão da forma ativa da NCC). Os coeficientes de prevalência nacionais são muito subestimados, embora em duas cidades do interior de São Paulo tenham sido verificados os valores de 72:100.000 e 96:100.000/ habitantes. Discutem-se aspectos relacionados à subestimação da prevalência desta neuroparasitose no Brasil. Cisticercose, infecção pela forma larvária metacestóide do parasita Taenia solium, desencadeando reações inflamatórias tanto ao redor do parasita como à distância do mesmo, é um grave e negligenciado problema de Saúde Pública. Os embriões podem alcançar qualquer tecido, porém mostram um grande tropismo (79-96%; mediana= Md= 89%) pelo sistema nervoso central (SNC) 1,2 . A manifestação, ou não, de sintomas é resultante da interação parasita-hospedeiro e depende da intensidade na resposta inflamatória do hospedeiro. . . PALAVRAS-CHAVE. . Os fatores que contribuem para a natureza endêmica do complexo teníase/cisticercose são muitos e complexos, mostrando estreita relação de dependência com os há-bitos de higiene pessoal, familiar e ambiental. Antecedente de teníase familiar é verificado em 22-34% dos pacientes com NCC, embora a positividade do exame coproparasitológico para Taenia sp. seja detectada em apenas 0-1,7% (Md= 1,3%) dos pacientes e em 4,3-5,4 % de seus familiares 1,[3][4][5] . A prevalência desta neuroparasitose, no Brasil, não está definida.Na literatura brasileira, as informações sobre NCC constituem coleção de trabalhos regionais que descrevem os aspectos polimórficos desta patologia. Os

The present study analyzed the (ICHD I-1988) and (ICHD II-2004) diagnostic criteria in children and adolescents. Our population consisted of 496 patients of the Headache Outpatient Ward for Children and Adolescents retrospectively studied from 1992 to 2002. Individuals were classified according to three diagnostic groups: Intuitive Clinical Diagnosis (Gold Standard), ICHD I-1988 and ICHD II-2004. They were statistically compared using the variables: Sensitivity (S), Specificity (Sp), Positive Predictive Value (PPV), Negative Predictive Value (NPV). When ICHD I-1988 was used, the sensitivity of migraine without and with aura was 21% and 27%, respectively, whereas in ICHD II-2004 it changed to 53% and 71% without affecting specificity. As a conclusion, the current classification criteria (ICHD II-2004) showed greater sensitivity and high specificity for migraine than ICHD I-1988, although it improved migraine diagnosis in children and adolescents, the sensitivity remains poor.

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-Study of 22 patients with the severe form of neurocysticercosis treated with albendazole (ABZ) administered in 6 different schedules ranging from 15 to 30 mg/kg/day for 21 to 60 days. Dextrochloropheniramine and ketoprofen were the adjuvant drugs. Multiple symptoms were observed in 90.9% of patients. Intracranial hypertension was manifested in 90.9%. Hydrocephaly occurred in 86.4%. Evolution was satisfactory in 10 patients, 8 died and 4 had sequelae. Tomographic studies showed the appearance of an isolated IV th ventricle in 9 patients, after ventriculoperitoneal shunt, before ABZ treatment in 3 of them, during in 5 and after treatment in one. Median clinical follow-up duration was 10 months for the patients who died and 3-4 years for survivors. In 3 patients there was an increase in cyst size during the administration of the 15 mg/kg/day ABZ dose, which was not observed in any patient when the 30 mg/kg/day dose was used.KEY WORDS: cysticercosis, neurocysticercosis, severe forms, treatment, albendazole, dextrochloropheniramine, ketoprofen. Formas graves da neurocisticercose: tratamento com albendazolRESUMO -Estudo de 22 doentes, com a forma grave de neurocisticercose, tratados com albendazol (ABZ), administrado em 6 diferentes esquemas, que variaram de 15 a 30 mg/kg/dia, durante 21 a 60 dias. A dextroclorofeniramina e o cetoprofeno foram as drogas coadjuvantes. Múltiplos sintomas ocorreram em 20 doentes. Hipertensão intracraniana foi manifestação mais comum em 20. Hidrocefalia foi detectada em 19. A evolução foi satisfatória em 45,4%, faleceram 36,4% e 18,2% ficaram com sequelas. Na evolução tomográfica apareceu IV o ventrículo isolado em 40,9%, após derivação ventriculoperitoneal, em 3 deles antes do tratamento com ABZ, em 5 durante e, em um, após o tratamento. A mediana estatística do período de seguimento clínico foi 10 meses para aqueles que faleceram e 3-4 anos para os sobreviventes. Em 3 doentes houve aumento no tamanho dos cistos durante a dose de 15 mg/kg/dia de ABZ, não observado na vigência de 30 mg/kg/dia. PALAVRAS-CHAVE: cisticercose, neurocisticercose, formas graves, tratamento, albendazol, dextroclorofeniramina, cetoprofeno.

SummaryWe tested the possible diagnostic utility of five Taenia saginata oncosphere-derived synthetic peptides in T. solium neurocysticercosis (NC). The five peptides correspond to protein sequences with high antigenic indexes that were cloned from a T. saginata oncosphere cDNA library. The test samples consisted of cerebrospinal fluid (CSF) samples randomly collected from patients referred from Mexican and Brazilian neurological institutes. Indirect enzyme-linked immunosorbent assays (ELISA) were carried out with the peptides either unconjugated or coupled to carrier proteins, and were compared with results obtained using T. solium cyst fluid as a positive control. For active inflammatory NC, the higher sensibility (93%) and specificity (85%) was obtained with peptides HP6-2 and Ts45W-1, respectively, coupled to ovalbumin, in both Mexican and Brazilian patients. Examining the results of the individual peptide assays in combination, in some instances, improved the sensitivity to 100%.

Neurocysticercosis (NCC) is an infection of the central nervous system (CNS) caused by the metacestode larval form of the parasite Taenia sp. Many factors can contribute to the endemic nature of cysticercosis. The inflammatory process that occurs in the tissue surrounding the parasite and/or distal from it can result from several associated mechanisms and may be disproportionate with the number of cysts. This discrepancy may lead to difficulty with the proper diagnosis in people from low endemic regions or regions that lack laboratory resources. In the CNS, the cysticerci have two basic forms, isolated cysts (Cysticercus cellulosae=CC) and racemose cysts (Cysticercus racemosus=CR), and may be meningeal, parenchymal, or ventricular or have a mixed location. The clinical manifestations are based on two fundamental syndromes that may occur in isolation or be associated: epilepsy and intracranial hypertension. They may be asymptomatic, symptomatic or fatal; have an acute, sub-acute or chronic picture; or may be in remission or exacerbated. The cerebrospinal fluid (CSF) may be normal, even in patients with viable cysticerci, until the patients begin to exhibit the classical syndrome of NCC in the CSF, or show changes in one or more routine analysed parameters. Computed tomography (CT) and magnetic resonance imaging (MRI) have allowed non-invasive diagnoses, but can lead to false negatives. Treatment is a highly controversial issue and is characterised by individualised therapy sessions. Two drugs are commonly used, praziquantel (PZQ) and albendazole (ABZ). The choice of anti-inflammatory drugs includes steroids and dextrochlorpheniramine (DCP). Hydrocephalus is a common secondary effect of NCC. Surgical cases of hydrocephalus must be submitted to ventricle-peritoneal shunt (VPS) immediately before cysticidal treatment, and surgical extirpation of the cyst may lead to an absence of the surrounding inflammatory process. The progression of NCC may be simple or complicated, have remission with or without treatment and may exhibit symptoms that can disappear for long periods of time or persist until death. Unknown, neglected and controversial aspects of NCC, such as the impaired fourth ventricle syndrome, the presence of chronic brain oedema and psychic complaints, in addition to the lack of detectable glucose in the CSF and re-infection are discussed.

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