Early neurologic complications following allogeneic bone marrow transplant for leukemia

Antonini, Giovanni; Ceschin, V.; Morino, Stefania; Fiorelli, Marco; Gragnani, F.; Mengarelli, Andrea; Iori, A. P.; Arcese, William

doi:10.1212/wnl.50.5.1441

Cited by 116 publications

(86 citation statements)

References 12 publications

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“…[1][2][3][4][5]10 The present study focused on the frequency and cause of opportunistic CNS infections in a large population of patients who had undergone BMT or PBSCT. A frequency of 4% of CNS infections after BMT or PBSCT in our population is comparable to that in former studies.…”

Section: Discussionmentioning

confidence: 99%

Opportunistic CNS infection after bone marrow transplantation

Maschke

Dietrich

Prumbaum³

et al. 1999

Bone Marrow Transplant

131

100

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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

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Section: Discussionmentioning

confidence: 99%

Opportunistic CNS infection after bone marrow transplantation

Maschke

Dietrich

Prumbaum³

et al. 1999

Bone Marrow Transplant

131

100

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“…2,3 Early complications, such as encephalopathy, cerebrovascular accidents, drug neurotoxicity and central nervous system (CNS) infections, have already been studied in detail. 4 In contrast, only limited information is available about neurological complications in the late phase after transplantation. Thus, the neurological manifestation of GVHD has been restricted to the motor endplate, skeletal muscle and peripheral nervous system, causing myasthenia gravis, polymyosistis and possibly polyneuropathy.…”

Section: Introductionmentioning

confidence: 99%

Cerebral angiitis in four patients with chronic GVHD

Sostak

Eigenbrod

et al. 2009

Bone Marrow Transplant

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There is growing evidence that GVHD affects the central nervous system (CNS). In this study, we describe the longterm follow-up of four allogeneic BM recipients who developed cerebral angiitis-like disease probably due to GVHD. The patients developed focal neurological signs, cognitive deficits and/or coma in association with GVHD, 2-18 years after transplantation, following reduction of immunosuppressive therapy. Magnetic resonance imaging was variable, showing generalized brain atrophy, ischemic lesions or leukoencephalopathy. Diagnosis of cerebral angiitis was confirmed by histopathological analysis of bioptic brain tissue and response to immunosuppressive therapy. By means of immunohistochemistry and immunofluorescence, perivascular lymphomononuclear cerebral infiltrates were shown to express the adhesion receptor, CD11a, and the chemokine receptor, CCR5. Our findings imply that GVHD should be considered in the differential diagnosis of noninfectious angiitis-like disease of the CNS in long-term survivors after allogeneic BMT. Infiltrating cells, in analogy to typical target organs of GVHD such as skin or liver, expressed CD11a and CCR5. These findings could be of etiopathological, diagnostic and therapeutic relevance.

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“…chemotherapy (with or without chemical arachnoiditis), 4 radiation toxicity or relapse of the neoplastic disease. [5][6][7][8] In our patient, an infectious, neoplastic, paraneoplastic or mechanical origin was improbable, based on the CSF and magnetic resonance imaging findings. Toxicity due to systemic or i.t.…”

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confidence: 72%