Korean J Pediatr 2011;54(1):40-45 • DOI: 10.3345/kjp.2011.54.1.40 43 on DWI (cytotoxic edema). At MRA, moderate to severe vessel irregularity consistent with vasoconstriction and vasodilation has been described in most patients, with reversal of vasoconstriction and vasodilation in nearly all patients4). Catheter angiography, MR A and MR perfusion (MRP) de- monstrate evidence of vasculopathy with focal and diffuse vaso- constriction, vasodilatation, and a string-of-bead pattern along with reduced relative cerebral blood volume in PRES patients1). Brain SPECT shows the underlying cerebral blood flow and consequently metabolic activity patterns of the brain. Diffusion tensor imaging (DTI) is a recently developed technique by virtue of its ability to visualize water diffusion characteristics and very useful to evaluate the extent of the fiber damage in diseases that affect the white matter. DTT, derived from DTI, allows for three- dimensional visualization of the architecture and integrity of the white matter tract at the subcortical level. DTT is more sensitive to explain the character of white matter lesions which cannot be explained by conventional MRI22-24). Rigorous and meticulous control of blood pressure is mandatory for successful treatment. Using various antihypertensive drugs, nicardipine is effective to limit blood pressure promptly with less f luctuation2, 17). Cessation of calcineurin inhibitor use is a key component. Most were reversible by reducing the dosage or withholding the drugs, but some reports showed successful control without cessation2). Symptomatic treatment measures and antipsychotic medication for possible psychotic stages, as in this case, may be needed. Also, aggressive, comprehensive early rehabilitation improves prognostic outcomes. The prognosis of PRES generally accepted as benign, except with intracranial hemorrhage. Recurrence is rare, but prolonged seizures, hypertension, or both may result in permanent neurological deficit and cerebral infarction2, 8, 18). If the intervention is not done in a timely manner, the functional vasogenic brain edema may convert to cytotoxic brain edema, giving permanent sequelae15). This case, after tacrolimus adminstration, presenting with sudden onset of neurologic symptoms, hypertension, and psychiatric symptoms showed improvement after cessation of tacrolimus and blood pressure control. Conventional MRI showed ischemic infarction, which could not explain the development of right-sided hemiplegia. However, using DTI, visualization was possible through DTT of white matter tract. References 1) Bartynski WS, Boardman JF. Catheter angiography, MR angiography, and MR perfusion in posterior reversible encephalopathy syndrome. Am J Neuroradiol 2008;29:447-55. 2) Ishikura K, Ikeda M, Hamasaki Y, Hataya H, Shishido S, Asanuma H, et al. Posterior reversible encephalopathy syndrome in children: its high prevalence and more extensive imaging findings. Am J Kidney Dis 2006;48:231-8. 3) Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500. 4) Hodnett P, Coyle J, O'Regan K, Maher MM, Fanning N. PRES (posterior reversible encephalopathy syndrome), a rare complication of tacrolimus therapy. Emerg Radiol 2009;16:493-6. 5) Ikeda M, Ito S, Hataya H, Honda M, Anbo K. Reversible posterior leukoencephalopathy in a patient with minimal-change nephrotic syndrome. Am J Kidney Dis 2001;37:E30. 6) Ikeda M, Yata N, Kamei K, Mori K, Ishikura K, Hataya H, et al. Posterior leukoencephalopathy syndrome in pediatric patients with kidney disease. Pediatr Nephrol 2002;17:71. 7) Parvex P, Pinsk M, Bell LE, O'Gorman AM, Patenaude YG, Gupta IR. Reversible encephalopathy associated with tacrolimus in pediatric renal transplants. Pediatr Nephrol 2001;16:537-42. 8) Prasad N, Gulati S, Gupta RK, Kumar R, Sharma K, Sharma RK. Is reversible posterior leukoencephalopathy with severe hypertension completely reversible in all patients? Pediatr Nephrol 2003;18:1161-6. 9) Casey SO, Truwit CL. Pontine reversible edema: a newly recognized imaging variant of hypertensive encephalopathy? Am J Neuroradiol 2000;21:243-5. 10) Singh N, Bonham A, Fukui M. Immunosuppressive-associated leuko- encephalopathy in organ transplant recipients. Transplantation 2000; 69:467-72. 11) Kwon S, Koo K, Lee S. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Pediatr Neurol 2001;24:361-4. 12) Lamy C, Oppenheim C, Meder JF, Mas JL. Neuroimaging in posterior reversible encephalopathy syndrome. J Neuroimaging 2004;14:89-96. 13) Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000;356: 411-7. 14) Schwartz RB, Feske SK, Polak JF, DeGirolami U, Iaia A, Beckner KM, et al. Preeclampsia-eclampsia: clinical and neuroradiographic correlates and insights into the pathogenesis of hypertensive encephalopathy. Radiology 2000;217:371-6. 15) Onder AM, Lopez R, Teomete U, Francoeur D, Bhatia R, Knowbi O, et al. Posterior reversible encephalopathy syndrome in the pediatric renal population. Pediatr Nephrol 2007;22:1921-9. 16) Kemper MJ, Sparta G, Laube GF, Miozzari M, Neuhaus TJ. Neuro- psychologic side-effects of tacrolimus in pediatric renal transplantation. Clin Transplant 2003;17:130-4. 17) Schwartz RB. Hyperperfusion encephalopathies: hypertensive ence- phalopathy and related conditions. Neurologist 2002;8:22-34. 18) Abe K. Reversible posterior leukoencephalopathy syndrome. Intern Med 2004;43:900-1. 19) Furukawa M, Terae S, Chu BC, Kaneko K, Kamada H, Miyasaka K. MRI in seven cases of tacrolimus (FK-506) encephalopathy: utility of FLAIR and diffusion-weighted imaging. Neuroradiology 2001;43:615- 21. 20) Akutsu N, Iwashita C, Maruyama M, Ootsuki K, Ito T, Saigo K, et al.