42 MU Kim, et al. • A case of tacrolimus-induced encephalopathy after kidney transplantation Fig. 3. Mild reduction of uptake in both anterior cingulate gyrus and left thalamus. Fig. 4. Dif fusion tensor tractography ( DT T ) on day 29 shows discontinuation of right corticospinal tract (CST) at cortex (arrow); and at 4 months, regeneration of right CST, with thinning. tomography (SPECT) (Fig. 3) and tensor MRI for diffusion tensor tractography (DTT) (Fig. 4) were performed. The patient went under comprehensive rehabilitation. Tensor MRI showed improving status of multifocal infarcts at both cerebral hemispheres. SPECT showed reduction of perfusion in both cingulate gyrus and left thalamus. On day 42, improvement of left side hemiparesis was noted, and follow-up MRA showed improvement of cerebral artery stenosis. On day 56, the patient was discharged from hospital, with improvement of left hand function, and gait disturbance. At four months after transplantation, increased dysarthria, along with right hand tremor and clumsiness were noted. Tensor MRI showed atrophy at both centrum semiovale, with progression to encephalomalacia. There were no further aggravations during follow- up. Discussion Causative agents of PRES include immunosuppressives such as tacrolimus, cyclosporine, cisplatin, and erythropoietin, with the condition manifesting in such presentations as preeclampsia and eclampsia, acute glomerulonephritis, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome4). Severe hypertension with autoregulatory failure and forced hyperperfusion remains to be widely accepted1). The key pathophysiological process of this syndrome was identified as vasogenic edema2, 12, 13). A breakdown in cerebral autoregulation results in the leakage of fluid into the interststium, which is detected as vasogenic edema. In patients with PRES, myogenic response is blunted by either passive overdistension of the vessels due to elevations in blood pressure or direct toxic effects on the endothelium4). The abnormalities primarily affect white matter but the cortex can also be involved4). The posterior cerebral hemispheres are susceptible to the neurotoxicity of calcineurin inhibitors, especially the occipital lobes7). The posterior circulation is most vulnerable because of poor sympathetic innervation. Diffusion-weighted imaging (DWI) has been shown to be reliable in distinguishing vasogenic edema from cytotoxic edema4, 14). The mechanism by which calcineurin inhibitors lead to neuro- toxicity remains poorly understood. Both cyclosporine and tacrolimus decreased endothelial cell viability and increased permeability, which is consistent with impaired function of the blood-brain barrier. Both drugs inhibit P-glycoprotein, which could lead to enhanced brain distribution of theses drugs and neurotoxicity7). The encephalopathy associated with tacrolimus is multifactorial in origin. Known factors include changes in intracellular urea concentration in the brain, fluid overload, high blood levels of tacrolimus/cyclosporine, and inadequate blood pressure control7). PRES clinically presents with seizures, severe headaches, and mental and visual changes15). Risk factors include hypertension and calcineurin inhibitor administration, fluid retention, renal failure, and alteration in vascular permeability2). Discontinuation of tacrolimus may be considered as diagnostic tool, if symptoms persist or other complications warrant this approach16). Differential diagnosis of PRES has been reported as ischemic stroke, cerebral venous thrombosis, intracranial vasculitis, progressive multifocal leukoencephalopathy, X-linked adrenoleukodystrophy, acute disseminated encephalomyelitis, encephalitis caused by electrolyte disturbance, and encephalopathy of unknown origin2). Of the imaging modalities, MRI is most sensitive diagnostic study, and is preferred tool than CT. It is more accurate for diagnosis and gives better prediction of PRES outcomes. DWI and apparent diffusion coefficient (ADC) maps can reliably differentiate the changes from cytotoxic edema4). Typical findings show high signal intensity mainly in subcortical white matter in the posterior parietal and occipital lobes in T2-weighted and FLAIR sequences, whereas atypical findings show involvement of gray matter, frontal lobes, thalamus, brainstem, and cerebellum as well as restricted diffusion