ebv infections have diverse clinical manifestations including subclinical infection , infectious mononucleosis ( i m ) , and associations with malignancies such as nasopharyngeal carcinoma , burkitt lymphoma , hodgkin 's disease , and primary central nervous system lymphoma . numerous neurologic manifestations associated with ebv have been documented , including encephalitis , aseptic meningitis , transverse myelitis , guillain.barre syndrome , cranial nerve palsies , and seizures occurring alone or in the setting of infectious mononucleosis1,2 ) . neuroimaging studies of ebv encephalitis are normal in most patients , but there have been some reports of increased signal intensities in both basal ganglia , thalami , and brainstem area during the acute stages of the illness1 - 3 ) . however , little data regarding the neuroradiologic findings associated with subacute or chronic stages of ebv encephalitis have been reported in the medical literature4,5 ) . there have been several case reports of abnormal white matter lesions on successive brain magnetic resonance imaging ( mri ) following herpes simplex encephalitis ( hse ) regardless of clinical symptoms6 - 11 ) . but there has been no report demonstrating increased white matter signal intensities on serial mri following ebv encephalitis without clinical manifestations . we present a case of a 2-year - old - boy demonstrating asymptomatic white matter lesions during the chronic phase after ebv encephalitis . a 2-year - old - boy was admitted to our hospital with a 2-day history of decreased activity with gait disturbance . he had an 11-day history of coughing , rhinorrhea and 8-day history of fever prior to admission . , he was lethargic and his body temperature was 36.9. physical examination showed enlarged tonsils bilaterally with exudates . laboratory findings included a leukocyte count of 15,200/l ( segmented neutrophil 28.1% , lymphocyte 58.8% , and monocyte 11.5% ) , hemoglobin 11.3 g / dl , platelet count 439,000/l , serum sodium 139 meq / l , potassium 4.4 meq / l , chlorine 99 meq / l , blood urea nitrogen 8.0 mg / dl , creatinine 0.6 mg / dl , glucose 91 mg / dl , ammonia 34 mol / l , and plasma lactate / pyruvic acid 2.44/0.55 mmol / l . cerebrospinal fluid ( csf ) analysis was contaminated with blood due to a traumatic tap . csf analysis revealed red blood cell 330,000/l , white blood cell 100/l ( lymphocyte 75% ) , protein > 300 mg / dl , glucose 71 mg / dl , csf immunoglobulin ( ig ) g index 1.12 ( < 0.85 ) , with a negative results for oligoclonal band . brain mri revealed multiple high signal intensities in both basal ganglia and thalami ( fig . csf for ebv polymerase chain reaction ( pcr ) was positive and serologic testing was compatible with an acute ebv infection : positive for viral capsid antigen ( vca)-igm , negative for vca - igg , ebv early antigen ( ea)-igg , and ebv nuclear antigen ( ebna)-igg . csf pcr for herpes simplex type i , ii , mycoplasma pneumoniae , and mycobacterium tuberculosis were all negative . encephalitis was diagnosed by clinical and radiologic findings , and empirical intravenous antibiotics and acyclovir were administered , but stopped after the final negative csf results for microorganisms were obtained . he recovered gradually without neurologic deficits and was discharged after the 7th day of admission . at 5 weeks after the onset of illness , he revealed no neurological symptoms or deficits on examination . however , follow - up brain mri demonstrated new multiple high signal intensities in both periventricular white matter with interval disappearance of previous lesions on t2-weighted and fluid attenuated inversion recovery ( flair ) images ( fig . 2 ) . since he remained clinically silent during the follow - up period , no additional studies were performed and no treatments were initiated . serologic testing for ebv was compatible with recent past infection : positive for vca - igg , negative for vca - igm , ea - igg , and ebna - igg . brain mri performed at 1 year after onset of the disease showed complete disappearance of previous white matter abnormal signal intensities with no newly developed lesions ( fig . 3 ) . during the 1-year follow - up , the patient continued to remain healthy with no neurological deficits . ebv is a well - known pathogen for i m and a herpesviridae family member . ebv infections have various neurologic manifestations alone or accompanied by clinical features of im1 - 3 ) . according to one study on pediatric ebv associated encephalitis , ebv is one of the more common identifiable causes of acute childhood encephalitis and remains the most common agent mimicking hse2 ) . some reports have suggested it to be a relatively benign , self - limited disease with almost full recovery . others have documented the occurrence of various neurologic sequelae in a substantial number of cases2,3 ) . in one pediatric study , 40% had residual neurologic sequelae that included global impairment , autistic - like behavior , and focal paresis3 ) . most children have a benign clinical course without neurologic sequelae , but 10% have residual persistent deficits and a mortality rate of up to 10% has been reported1,2 ) . since ebv has a tropism for the deep nuclei , neuroimaging can show characteristic multiple foci of t2-weighted or flair hyperintensity in the hemispheric cortex , brainstem , bilateral thalami , basal ganglia , and/or splenium1 - 3,12,13 ) . rarely , extensive white matter lesions have been reported in patients with acute disseminated encephalomyelitis ( adem ) associated with chronic ebv infection and clinical relapse of neurologic problems4,5 ) . however , there have been no reports documenting sequential cranial mri findings in asymptomatic patients following ebv encephalitis . our patient suffered from ebv encephalitis coincidentally with i m and recovered completely without neurologic sequelae . he was followed up at our outpatient clinic regularly for close observation of neurologic complications . the follow - up brain mri was performed for the purpose of demonstrating resolution of initial deep nuclei lesions seen on presentation . however , his follow - up mri revealed extensive periventricular white matter hyperintensities resembling that of an adem patient . despite his multiple cerebral lesions on brain mri , subsequently , white matter lesions completely disappeared on the third brain mri one year later . although our patient could be diagnosed as having adem following ebv encephalitis according to the neuroradiologic features of his second brain mri , he did not display any evidence of encephalopathy or clinical features compatible with adem at that time . as a result , his neuroradiologic findings are believed to represent one spectrum of post infectious autoimmune - mediated demyelinating lesions . a secondary immune - mediated process has been suspected in some patients with transient or chronic white matter involvement occurring after hse . these patients were asymptomatic or developed an acute or chronic secondary neurologic deterioration without extrapyramidal movement disorder6 - 11,14 ) . though the exact mechanisms responsible for the transient white matter lesions observed after hse remain unclear , possible explanations include a postinfectious immune - mediated demyelination process or prolonged edema or gliosis induced by chronic stimulation of the immune system in response to viral infection6 - 11,14 ) . in addition , white matter lesions have also been noted to be related to intravenous acyclovir in some cases15 ) . this is the first report of a patient with transient diffuse white matter hyperintensities following ebv encephalitis in the absence of neurologic symptoms or signs . ebv is a family member of herpersviridae and is known to be the most common virus mimicking hse in clinically . as a result , the white matter lesions following ebv infection could also resemble that of hse . given that we did not pursue further studies after finding his new white matter lesions , potential limitations in accurately diagnosing this patient remains . since this was the first case report demonstrating a patient with asymptomatic self - limited white matter lesions during the chronic phase following ebv encephalitis , more clinical data and future research is needed to better characterize and determine the significance of our findings .
we present the case of a patient with epstein - barr virus ( ebv ) encephalitis who developed abnormal white matter lesions during the chronic phases of the infection . 
 a 2-year - old - boy was admitted for a 2 day history of decreased activity with ataxic gait . 
 the results of the physical examination were unremarkable except for generalized lethargy and enlarged tonsils with exudates . 
 brain magnetic resonance imaging ( mri ) at admission showed multiple high signal intensities in both basal ganglia and thalami . 
 the result of ebv polymerase chain reaction ( pcr ) of the cerebral spinal fluid was positive , and a serological test showed acute ebv infection . 
 the patient was diagnosed with ebv encephalitis and recovered fully without any residual neurologic complications . 
 subsequently , follow - up mri at 5 weeks revealed extensive periventricular white matter lesions . since the patient remained clinically stable and asymptomatic during the follow - up period , no additional studies were performed and no additional treatments were provided . at the 
 1-year follow - up , cranial mri showed complete disappearance of the abnormal high signal intensities previously seen in the white matter . 
 the patient continued to remain healthy with no focal neurologic deficits on examination . 
 this is the first case of asymptomatic self - limited white matter lesions seen in serial mri studies in a korean boy with ebv encephalitis .