INTRODUCTION Granulomatous inflammation is a distinctive ...

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enhance with contrast media on neuroimaging. As the parasite loses the ability to control the host immune response, an inflammatory process begins. Initially, the cysts show slight pericystic contrast enhancement. Later they become markedly inflamed and edematous and appear as ringlike or nodular areas of enhancement after the injection of contrast. This phase has been called "granulomatous cysticercosis, " or "enhancing lesions." Finally, the cyst is processed by the cellular response, and its remnants either are not detectable by imaging or become calcified lesions . "Giant" cysts, measuring more than 50 mm in diameter, are occasionally found, located primarily in the Sylvian fissure. Cysticercotic encephalitis is a rare form of the disease in which patients have numerous inflamed cysticerci, leading to diffuse, severe cerebral edema (Escobar, 1983; Kramer et al., 1989;.Dumas et al., 1997). Symptomatic disease results almost exclusively from the invasion of the nervous system (neurocysticercosis) and the eye and is clearly differentiated into parenchymal neurocysticercosis and extraparenchymal neurocysticercosis. The usual presentation of parenchymal neurocysticercosis is with seizures. Occasionally, the cysts may grow and produce a mass effect. Extraparenchymal infection may cause hydrocephalus by mechanical obstruction of the ventricles or the basal cisterns, either by the cysts themselves or by an inflammatory reaction (ependymitis and/or arachnoiditis). The so called racemose variety occurs in the ventricles or basal cisterns and is characterized by abnormal growth of cystic membranes with degeneration of the parasite's head (scolex). These cases follow a progressive course, and even after ventricular shunting, the membranes or inflammatory cells and proteins frequently block the shunt (Rabiela et al., 1989). Clinical picture In most patients, neurocysticercosis seems to produce symptoms years after the initial invasion of the nervous system (Del Brutto and Sotelo, 1988), by either inflammation around the parasite, mass effect, or residual scarring. There is a clear association between inflammation around one or more cysts and development of symptoms, especially with regard to seizures (White et al., 1997). The usual presentation of parenchymal neurocysticercosis is with seizures, which is either focal, focal with secondary generalization or generalized. Electroencephalographic (EEG) studies for patients with active disease may reveal focal abnormalities. The seizures are usually easily controlled with antiepileptic drug therapy (Carpio and Hauser, 2002). Headache is common among patients with Neurocysticercosis. It could be hemicranial or bilateral, and may be seen with parenchymal, ventricular or cisteranl involvement (Rajshekhar, 2000). Patients may also present with symptoms and signs of raised ICP. Symptoms may include nausea or vomiting, altered mental status, visual changes, or dizziness. The patients with cysticercal encephalitis may have altered mental status raised ICP, or seizures (Rangel et al., 1987). Diagnosis The diagnosis of neurocysticercosis is difficult because clinical manifestations are nonspecific, most neuroimaging findings are not pathognomonic, and some serologic tests have low sensitivity and specificity. A set of diagnostic criteria was proposed in 1996 and recently revisited (Del Brutto et al., 2001), based on objective clinical, imaging, immunological, and epidemiological data; these criteria consist of four categories that are stratified according to their diagnostic strength (Table 4). These criteria provide two degrees of diagnostic certainty. Definitive diagnosis, in patients who have one absolute criterion or in those who have two major plus one minor and one epidemiologic criteria; and probable diagnosis, in patients who have one major plus two minor criteria, in those who have one major plus one minor and one epidemiologic criteria, and in those who have three minor plus one epidemiologic criteria. This chart of diagnostic criteria for neurocysticercosis has not yet been tested in hospital-based studies (Del Brutto et al., 2001).
Table 4. Diagnostic criteria for neurocysticercosis (Del Brutto et al., 2001) Absolute Major Minor Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion Cystic lesions showing the scolex on CT or MRI Direct visualization of subretinal parasites by fundoscopic examination Lesions highly suggestive of neurocysticercosis on neuroimaging studies Positive serum immunoblot for the detection of anticysticercal antibodies Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel Spontaneous resolution of small single enhancing lesions Lesions compatible with neurocysticercosis on neuroimaging studies Clinical manifestations suggestive of neurocysticercosis Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens Cysticercosis outside the central nervous system Epidemiologic Evidence of a household contact with T. solium infection Individuals coming from or living in an area where cysticercosis is endemic History of frequent travel to disease-endemic areas Investigations Demonstration of T. Solium infection in biopsy or autopsy material makes a conclusive diagnosis but is rarely available. Also the parasites may be visualized directly during ophthalmologic examination, when there is ocular involvement(Cardenas et al., 1992). These are considered absolute criteria for diagnosis. Serology Antibody detection assays have proven problematic in cysticercosis because of cross reactions to other common parasites and nonspecific binding of antibody by the parasite. Thus assays that employ crude antigen have proven problematic. The immunoblot assay employing semipurified membrane antigens, termed enzyme-linked immunotranfer blot (EITB) provided better results
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