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(tacrolimus) are potent immunosuppressive agents that are widely used in organ transplantation of the kidney. However, these agents can induce neurotoxicity. The spectrum of neurological disturbances caused by calcineurin inhibitors ranges from very mild symptoms such as paresthesia, tremor, headache and flushing to severe changes that may cause a lethal outcome (1, 2). The neurotoxicity of these agents in the central nervous system has been increasingly reported with the widespread use of magnetic resonance imaging (MRI). FK506 leukoencephalopathy has been included within posterior reversible leukoencephalopathy syndrome (PRES), and this has also been caused by cyclosporine, eclampsia, malignant hypertension, renal failure and drug-induced thrombotic thrombocytopenic purpura. The MR finding of FK506-induced PRES are well documented and these include increased signal intensities in both parieto-occipital lobes on the T2-weighted images (T2WI), the diffusion-weighted images (DWI) and the apparent diffusion coefficient (ADC) mapping. These findings indicate vasogenic edema rather than cytotoxic edema (3, 4). However, reports about FK506-induced cerebral infarction are not common. We report here on a case of acute cerebral infarction after FK506 administration in a kidney transplantation recipient.

Acute Cerebral Infarction after FK 506 Administration in a Kidney Transplantation Recipient: A Case Report