There was a significant difference between each group (P < .001). A case is presented with central nervous system involvement. Thirty rats heterotopically underwent small bowel transplantation and were divided into 5 groups as follows: group A, syngraft (SYN) alone; group B, SYN with FK506; group C, SYN with FK506 and BBS; group D allograft with FK506; group E, allograft with FK506 and BBS. There were reversible low-attenuation changes on CT and bright T2-weighted signal changes on MRI in the cortex and/or white matter of the cerebral hemispheres. Multiplying extent by severity gave regional scores, which were summated to give an overall score. the posterior leukoencephalopathy syndrome are also documented. Tacrolimus-induced neurotoxicity is usually mani-fested as encephalopathy, but also a wide range of in-fectious or cerebrovascular complications might occur [6, 13]. Computed tomography (CT) is the initial choice of investigation, which is easily available and helps to exclude major intracranial abnormality such as haemorrhage. : Case Reports, Posterior Reversible Encephalopathy Syndrome Following Infliximab Infusion, Journal of Pediatric Gastroenterology and Nutrition, Severe neurologic side effects in patients being treated for hemophagocytic lymphohistiocytosis, Leukoencephalopathy with cerebral hemorrhage following acute pancreatitis due to tacrolimus in a case of allogeneic peripheral blood stem cell transplantation, Human herpesvirus-6 encephalitis after unrelated cord blood transplantation, PRES (posterior reversible encephalopathy syndrome), a rare complication of tacrolimus therapy, What Is the "Therapeutic Range" for Voriconazole?, Posterior Reversible Encephalopathy Syndrome, Part 1: Fundamental Imaging and Clinical Features, Neurological Complications of Hematopoietic Stem Cell Transplantation, Lysergic Acid Amide-Induced Posterior Reversible Encephalopathy Syndrome with Status Epilepticus, Neurotoxicity is a significant complication of the use of tacrolimus. CTs were read separately by 2 radiologists. Neurologic adverse effects are varied and manifest irrespective of tacrolimus levels. Imaging abnormalities were observed in five of six patients during the course of their neurologic illnesses. Tacrolimus was switched to cyclosporine. Mental status changes, cognitive deficits, seizures and lethargy were the most common clinical findings. In spite of difficult surgical procedures and the demand for a long-term immunosuppression, results for transplant patients have substantially improved over the last decades. More … From April 1998 to December 2001, we identified 10 patients (six women, four men) who developed 11 episodes of tacrolimus‐associated posterior reversible encephalopathy syndrome (PRES) after allogeneic haematopoietic stem cell transplantation for haematological malignancies. Aspergillus fumigatus and Aspergillosis, Diagnostic and therapeutic implications of neurological complications following paediatric haematopoietic stem cell transplantation, In cyclosporine induced neurotoxicity, is tacrolimus an appropriate substitute or is it out of the frying pan and into the fire?, Posterior Reversible Encephalopathy Syndrome (PRES) in a Thirty-Six-Week Gestation Eclamptic, Central Nervous System Complications after Allogeneic Hematopoietic Stem Cell Transplantation: Incidence, Manifestations, and Clinical Significance, Tacrolimus-related nocturnal myoclonus of the lower limbs in elderly patients with rheumatoid arthritis, Posterior reversible encephalopathy syndrome due to sirolimus, Two cases of progressive multifocal leukoencephalopathy after allogeneic hematopoietic cell transplantation and a review of the literature, Fourteen patients receiving CsA after allogeneic bone marrow transplantation or with marrow aplastic disorders developed neurotoxicity and MR or CT imaging abnormalities. Tacrolimus was started at a median of 8 wk (range 10 d to 8.7 yr) after RTPL and was continued for a median of 2.5 yr (range 5 wk to 4.6 yr). For each patient, neurologic symptoms began when the tacrolimus level in blood was at a peak, exceeding the therapeutic limit in all but one case. FK506 causes severe neurotoxicity in transplanted grafts, and BBS protects graft enteric ganglia against the neurotoxic effects of FK506.Neurotoxicity is a recognized complication with the use of Cyclosporin A (CSA) in bone marrow and organ transplantation patients.