Summary:We retrospectively identified opportunistic CNS infections in 655 patients who had undergone allogeneic, syngeneic or autologous BMT or PBSCT between 1990 and 1997. Twenty-seven patients (4%) developed CNS infections. All CNS infections occurred in allogeneic BMT or PBSCT patients. The most common CNS infections were toxoplasma encephalitis (74%) and cerebral aspergillosis (18%). Furthermore, we identified one patient with candida encephalitis and one patient with viral encephalitis. Overall mortality of patients with opportunistic CNS infection was 67%. There were two different groups of toxoplasma encephalitis with a different appearance on MR imaging. The first group showed edema, but no gadolinium enhancement, whereas the second group exhibited typical MRI appearances with the exception of frequent hemorrhagic transformation. The first group had a significant shorter latency between BMT and onset of CNS infection (mean 45 days vs 180 days, P = 0.02), a significant higher daily dose of corticosteroids as treatment for graft-versus-host disease (GVHD) (P = 0.01), more severe GVHD and a higher mortality (71% vs 36%). This study shows that the most common CNS infections in our patient population are toxoplasma encephalitis and cerebral aspergillosis, that there are two distinct subgroups of toxoplasma encephalitis and that CNS infections occur after allogeneic BMT only. Keywords: CNS infection; cerebral toxoplasmosis; cerebral aspergillosis Both allogeneic and autologous BMT are associated with several neurologic complications secondary to the underlying disease and prolonged myelosuppression. [1][2][3][4] The use of immunosuppressive drugs such as corticosteroids and cyclosporine in order to avoid rejection of the allograft and to control graft-versus-host disease (GVHD) is another major risk factor for neurologic complications especially CNS infections. In previous studies the most common complications were cerebral hemorrhage, metabolic encephalopathy and CNS infection. 1-5 Neurologic complications were more frequent in patients when AML was the underlying disease than in other leukemia patients. 4