Korean J Pediatr 2011;54(1):40-45 • DOI: 10.3345/kjp.2011.54.1.40 41 shows edema involving the white matter in the posterior portions of the cerebral hemispheres, especially bilaterally in the parieto-occipital regions2, 3). Prompt recognition is vital, as most patients will experience complete recovery by reduction of drug dosage or by withholding the immunosuppressive agent altogether4). Symptomatology and characteristic MRI features of this clinicoradiological entity have been reported, but it still is poorly understood by pediatricians5-11). Here, we present a case of tacrolimus-induced encephalopathy which was visualized through diffuson-tensor tractography. Case report An eleven-year old girl has had chronic renal insufficiency since her neonatal period. She was born premature at 32 weeks gestation, diagnosed with renal hypoplasia, hypocalcemia, neonatal sepsis, urinary tract infection, acute renal failure, and atrial septal defect during neonatal period. She has been under conservative treatment (erythropoietin, angiotensin-converting enzyme (ACE) inhibitors, and calcium) without dialysis since then. At the age of 11 years, she received kidney transplantation from her mother, a preemptive living related donor kidney. There were two HLA-B, and HLA-DR mismatches but ABO-identity (O positive). Immunosuppression included tacrolimus (0.1 mg/kg/day, bid), mycophenolate mofetil (600 mg/m2, bid), and prednisolone (0.5 mg/kg qd). Postoperatively, her renal function was good without acute rejection. On day 12 after transplantation, sudden onset of left side motor weakness of grade 0 developed. Blood pressure was 160/100 mmHg and consequently, antihypertensive drugs were administered. Brain magnetic resonance imaging (MRI) and angiography (MRA) showed acute infarction at right frontal lobe of middle cerebral artery territory (Fig. 1, 2). Other laboratory findings were normal, including serum creatinine of 0.69 mg/dL. Serum tacrolimus level was 9 ng/ mL. On day 13, psychiatric symptoms such as irritability, mood instability, aggressive behavior, and dysarthria developed, diagnosed as adjustment disorder, antipsychotics medication started. Within few days, psychotic symptoms improved. On day 19, mentality and blood pressure were restored, with slight improvement of left hemiparesis of grade 1 to 2. Follow-up MRI was taken after some clinical improvement, showing new infarct lesions at both cerebral hemispheres. Tacrolimus dose was reduced. But with no recognizable clinical response even after decreased serum concentration, it was replaced by cyclosporine. On day 29, her renal function was normal, and her blood pressure was normotensive. Brain single photon emission computed Fig. 1. High-signal intensity at right frontal lobe affecting mainly white matter in T2-weighted images on day 12, was bright on diffusion-weighted images and low-intensity on ADC maps, consistent with cytotoxic edema, suggesting acute cerebral infarction (arrows). Fig. 2. Angiography showed severe stenosis at both anterior (ACA) and middle cerebral arteries (MCA), with minimal stenosis at both posterior cerebral arteries (arrows).