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Accepted 20 March 1980 Over the next three months his hemiparesis improved but not completely.In July, 1978, the patient had a sudden exacerbation of the left hemiparesis associated with headache. Neurological evaluation demonstrated only left hemiparesis and hyperreflexia. The leg was more involved than the arm and was more impaired distally than proximally. A repeat CT scan without contrast showed a diffuse high density lesion consistent with the presence of blood within the previously demonstrated tumour mass (fig 2). Progression of the left hemiparesis led to surgical exploration At surgery an egg-shaped tumour was found attached to the falx. The superior sagittal sinus was patent. Tissue necrosis and yellow discoloration due to previous haemorrhage were found within the tumour capsule. The adjacent motor cortex was atrophic, but there was no evidence of either recent or old intracerebral or subdural haemorrhage. Approximately 95 % of the necrotic tumour was resected, leaving only a small portion attached to the falx at its inferior aspect next to the corpus collosum.

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The nature of inflammatory lymphocytes recruited to the CNS has been studied in a model of chronic inflammation. Injection of killed Corynebacterium parvum into the cortex of the mouse brain produces a circumscribed inflammatory cellular infiltrate around the injection site, and recruited mononuclear inflammatory cells (IC) can be isolated for flow cytometric analysis. The majority of IC were T cells. In comparison with the predominant naive population of mesenteric lymph node T cells, IC T cells express much higher levels of CD44, LFA-1 and ICAM-1, and lower levels of CD45RB, features commonly associated with memory (previously activated) cells. In addition, in contrast to the L-selectin+ alpha 6-integrinlow phenotype of naive lymph node T cells, IC T cells lacked L-selectin and were alpha 6-integrin-. Mac-1, recently proposed as another marker of memory T cell differentiation, was not displayed by IC T cells, suggesting that Mac-1 expression may be heterogeneous among memory T cell subsets. A subset of mesenteric lymph node (MLN) T cells, probably representing activated T cells undergoing the naive to memory transition, but not of IC T cells, expressed high levels of alpha 6-, beta 7- and alpha E-integrin. IC and MLN naive T cells expressed comparable levels of alpha 4-integrin, but IC T cells stain poorly with anti-beta 7 mAbs and with mAb DATK 32, specific for the alpha 4 beta 7 heterodimeric lymphocyte homing receptor for the mucosal addressin MAdCAM-1, suggesting that these inflammatory cells express more alpha 4 beta 1 than alpha 4 beta 7. Consistent with this, in in vitro adhesion assays, brain IC bound better than MLN cells to the alpha 4 beta 1 integrin ligand VCAM-1 and the LFA-1 ligand ICAM-1 but adhered very poorly to the alpha 4 beta 7 ligand MAdCAM-1. These findings are consistent with and extend previous immunohistological studies of T cells in murine experimental autoimmune encephalomyelitis, and demonstrate a distinctive phenotype for lymphocytes being present in the chronically inflamed brain.

Resistance against acute and chronic infection with Toxoplasma gondii in BALB/c and CBA/Ca mice was compared. Intraperitoneal inoculation ofeither 20, 40, or 80 cysts of the ME49 strain resulted in mortality rates in BALB/c mice of 12% (2 of 17), 50% (6 of 12), and 75% (9 of 12), respectively, within 3 weeks after infection (acute stage). There was no mortality in the CBA/Ca mice for any of the doses. In marked contrast, CBA/Ca mice were highly sensitive to chronic infection with developing toxoplasmic encephalitis; they began dying 2 months after infection with 10 cysts of the ME49 strain, and mortality reached 53% (16 of 30) by the sixth month postinfection. No mortality (0 of 20) was observed in the chronically infected BALB/c mice. CBA/Ca mice had markedly more cysts in their brains than BALB/c mice in the chronic stage. Severe inflammatory changes were observed only in the brains of CBA/Ca mice. Interestingly, in the acute stage (the first 3 weeks), numbers of cysts in the brains were significantly greater in CBA/Ca than BALB/c mice, whereas only BALB/c mice showed mortality in that time period. No inflammatory changes were observed in brains of BALB/c mice during the acute stage of the infection. Thus, resistance against chronic infection appears to be regulated by a mechanism(s) that is different from those conferring resistance against acute infection. There was no difference in gamma interferon levels in sera between CBA/Ca and BALB/c mice during the acute stage. However, during the chronic stage, only BALB/c mice had detectable levels of gamma interferon in their sera.

Treatment of toxoplasmic encephalitis in C57BIJ6 mice with monoclonal antibody (MAb) against interleukin-6 (IL-6) resulted in a remarkable decrease in the number of foci of acute inflammation in their brains caused by proliferation of tachyzoites. In brains of mice treated with isotype control MAb and those treated with anti-IL-6 MAb, tachyzoites were observed only in foci of acute inflammation. Immunoperoxidase staining revealed a greatly diminished frequency of tachyzoites in brains of mice treated with anti-IL-6 MAb. Of interest, treatment with MAb against IL-6 was also associated with reduced numbers of Toxoplasma gondii cysts in the brains and with higher serum levels of gamma interferon than in control mice. Paradoxically, the mice treated with anti-IL-6 MAb had higher serum levels of IL-6 as measured by an enzyme-linked immunosorbent assay than controls. These results revealed the importance of IL-6 in the immunopathogenesis of murine toxoplasmic encephalitis.