MR studies of 6 patients with intracranial tuberculoma are reviewed. All patients also underwent CT scans which showed hypo- or isodense lesions with abnormal enhancement following contrast administration. MR showed lesions with prolongation of the T1 relaxation time in every case. On the T2-weighted sequences, the signal properties of the tuberculoma varied according to the stage of evolution of the lesion. Incipient tuberculomas appeared as scattered areas of hypointensity surrounded by edema. Mature tuberculomas were composed of a dark necrotic center surrounded by an isointense capsule which was, in turn, surrounded by edema. In one patient, the center of the lesion was hyperintense probably because of liquefaction and pus formation (tuberculous abscess). While both, CT and MR, were equally sensitive in visualizing the intracranial tuberculoma in every patient, MR was slightly superior in demonstrating the extent of the lesion, especially for brainstem tuberculomas. Nevertheless, the potential role for MR diagnosis of intracranial tuberculoma is limited by the fact that other infectious or neoplasic diseases may present similar findings. The diagnosis of intracranial tuberculoma should rest on a proper integration of data from clinical manifestations, cerebrospinal fluid analysis, and neuroimaging studies.
SUMMARY
Sixteen cysticerci excised from 15 surgery patients were examined for the presence of HLA molecules on their surface, to confirm the role of these molecules in parasite damage and to investigate if HLA products are host specific or perhaps host‐like antigens synthesized by the parasite. MoAbs against monomorphic and polymorphic HLA were chosen according to the patients HLA phenotypes. MoAbs against host and non‐host antigens were selected and tested on cyst slides by indirect immunofluorescence assays. Host molecules were present in 43.7% of the cysts, but non‐host antigens were also apparent in 62.5%. These results suggest mimicry as a possible mechanism to explain the presence of MHC products on the surface of the parasite; inflammation may also induce the expression of HLA that could become associated with the parasite. In vitro cellular immune response to specific antigens was also performed and positive responses correlated with the presence of HLA molecules on the cyst's surface. Moreover, damaged parasites had host molecules as well. Parasites from responder patients had all kind of HLA molecules or at least, antigenic determinants while the cysts from non‐responders did not have molecules on their surface. These data support the role of HLA in cyst destruction.
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