This article reviews the pathology of human spinal cord injury (SCI), focusing on potential differences between humans and experimental animals, as well as on aspects that may have mechanistic or therapeutic relevance. Importance is placed on astrocyte and microglial reactions. These cells carry out a myriad of functions and we review the evidence that supports their beneficial or detrimental effects. Likewise, vascular responses and the role of inflammation and demyelination in the mechanism of SCI are reviewed. Lastly, schwannosis is discussed, highlighting its high frequency and potential role when designing therapeutic interventions. We anticipate that a better understanding of the pathological responses in the human will be useful to investigators in their studies on the pathogenesis and therapy of SCI.

In a large cohort of renal allograft recipients, PTLD affected 1%. Disease localized near the allograft was the most common variant. For most patients with localized disease, the outcome was graft loss, and the mortality was low. Localized PTLD should be considered in the differential diagnosis of allograft dysfunction in the 1st posttransplant year.

The occurrence of posttransplant lymphoproliferative disorder (PTLD) in solid organ allograft recipients can be quite varied in clinical presentation, histopathological characteristics and frequency. A variety of lymphomas can develop as a PTLD although some types appear infrequently and remain poorly understood in this clinical setting. In this report, we describe two cases of Burkitt s lymphoma presenting as a PTLD following liver transplantation. The recipients were 12 and 44 years of age and displayed gastrointestinal involvement by the tumors several years following transplant. The tumors displayed the typical histological features of Burkitt s lymphoma and were markedly positive for EBV. The tumors displayed similar immunophenotypic characteristics by flow cytometry and had rearrangements of the immunoglobulin J-H heavy chain. The tumors required aggressive chemotherapy and a cessation of immunosuppressive therapy. This report demonstrates that Burkitt s type lymphomas can develop in the posttransplant setting and that these tumors contain morphologic, cytofluorographic and molecular features identical to Burkitt s lymphomas that occur in non-transplant patients. Our experience is that these PTLD- Burkitt s lymphomas behave aggressively and require intensive chemotherapeutic intervention.

Posttransplantation lymphoproliferative disorder may be limited to the allograft. A focal complex mass in the renal allograft hilum surrounding the main renal blood vessels is a common finding and can be visualized with sonography. MR imaging can help increase diagnostic confidence.