reversible focal lesions in the splenium of the corpus callosum ( scc ) have been found in patients with various conditions including seizures , antiepileptic drug toxicity or withdrawal , viral encephalitis , hypoglycemia , wernicke 's encephalopathy , marchiafava - bignami disease , sympathomimetic - induced kaleidoscopic visual illusion syndrome , hemolytic uremic syndrome , altitude brain injury , and acute axonal injury .
analysis of the current literature revealed that the most frequent cause of reversible focal lesions of the scc is influenza virus - associated encephalitis / encephalopathy ( iaee ) .
the abnormality has been reported in association with various viruses ( e.g. , epstein - barr virus , rotavirus , influenza virus ) ( 1 - 3 ) .
the brain lesions described in patients with iaee include restricted diffusion involving the cerebral cortex and subcortical white matter in various locations , symmetric lesions in the brainstem , basal ganglia , thalamus , and cerebellar white matter with or without brain edema , and mild brain atrophy .
transient restricted diffusion of the scc in patients with iaee has also been described ( 4 ) . here ,
we report an adult who presented with non - specific dizziness and lesions of the scc on magnetic resonance imaging ( mri ) who was diagnosed with hemorrhagic fever with renal failure syndrome ( hfrs ) with serologically proven hantaan virus infection .
a previously healthy 53-yr - old man presented with a 6 - 7-day history of fever up to 40 and dizziness .
the initial diffusion - weighted images revealed high signal intensity in the corpus callosum with a low signal on the apparent diffusion coefficient ( adc ) map ( fig .
1 ) . the next day , he developed thrombocytopenia ( 4010/l ) and was transferred to our emergency room for further evaluation .
he stated that he had been tying rice straw into sheaves several days earlier , but not using any drugs , like metronidazole , antiepileptic drug or alcohol , and had not been exposed to toxins or experienced weight loss . on neurologic examination , he was slightly confused , and scored 24/30 on the mini mental status exam ( mmse ) .
the cranial nerve , motor , and sensory examinations , deep tendon reflexes , and cerebellar function tests were normal .
his blood tests showed marked thrombocytopenia ( 2110/l ) and azotemia ( bun / cr 23 mg / dl/1.5 mg / dl ) .
he was started on cefotaxime and clindamycin for a suspected infection and transfused with fresh frozen plasma , but his fever ( > 38.0 ) was sustained .
two days after admission , he was alert and his fever had subsided , but the oliguria , azotemia ( bun / cr 49 mg / dl/3.0 mg / dl ) , and thrombocytopenia ( 610/l ) had worsened ( figs . 2 , 3 ) .
four days later , the thrombocytopenia had recovered , although the azotemia ( bun / cr 82 mg / dl/7.1 mg / dl ) had not improved .
he was diagnosed with hfrs based on the detection of hantaan virus antibody in his serum .
six days later , he was alert , and his electroencephalograph ( eeg ) was normal . his platelet count had stabilized ( 31110/l ) , and a lumbar puncture was performed .
the cerebrospinal fluid ( csf ) analysis revealed no cells , a nor mal protein level of 26.0 mg / l , a normal glucose level of 80 mg / dl , and no organisms on gram staining .
the mri findings had resolved completely in follow - up studies conducted on day 14 ( fig .
hemorrhagic fever with renal failure syndrome occurs mainly in europe and asia and is characterized by a fever and renal failure associated with hemorrhagic manifestations .
hfrs is caused by airborne contact with secretions from rodent hosts infected with viruses belonging to the genus hantavirus in the family bunyaviridae .
the clinical features consist of a triad of fever , hemorrhage , and renal insufficiency ( 5 ) .
other common symptoms during the initial phase of the illness include , myalgia , abdominal and back pain , and diarrhea . in most cases , mild neurological symptoms such as headache , vertigo , and nausea
the pathogenesis is largely unknown , but findings from several studies have suggested that immune mechanisms play an important role .
after the infection , marked cytokine production , kallikrein - kinin activation , complement pathway activation , and increased levels of circulating immune complexes occur .
damage to the vascular endothelium , capillary dilatation , and leakage are clinically significant features of the disease .
myelin sheaths in the scc have a relatively high water component , and the scc is more susceptible to cytotoxic edema than are other brain areas ( 2 ) .
reversible brain lesions have been attributed to the transient development of intramyelinic edema due to the separation of myelin layers , which is a possible mechanism for the transiently decreased diffusion of the scc lesion ( 2 , 11 ) .
the influx of inflammatory cells and molecules , possibly combined with related cytotoxic edema , might have decreased the adc ( 2 , 12 , 14 ) .
the most common causes of reversible focal lesions of the scc are viral encephalitis , antiepileptic drug toxicity / withdrawal , and hypoglycemic encephalopathy .
they are not specific to iaee and have been reported secondary to various infectious agents , including rotavirus , measles , herpesvirus , salmonella organisms , mumps , varicella - zoster virus , adenovirus , o157 escherichia coli - associated hemolytic - uremic syndrome , legionnaires ' disease , and unknown pathogens ( 4 , 9 , 14 ) .
the similar clinical and imaging features suggest a common mechanism induced by different pathological events leading to the same results ( 1 ) .
the most likely causes of these transient lesions of the scc have been explained as a rapidly resolving intramyelinic infiltrate or the influx of inflammatory cells and macromolecules , combined with related cytotoxic edema , which is very similar to the pathogenesis of hfrs ( 2 , 7 , 9 , 10 , 13 ) .
this argues for a non - specific cause related to vasogenic edema , probably secondary to the inflammatory response ( 2 , 7 ) our patient was diagnosed with hfrs , and his mri showed scc lesions .
we report a reversible scc lesion associated with hfrs . to our knowledge , this is the first case of virus - associated encephalitis / encephalopathy in which the pathogen was a hantaan virus .
although it is not certain whether the neurologic symptoms in this patient might have been caused by fever , or scc lesions , or both , we suggest that hfrs patients with neurologic symptoms like dizziness and mental slowing should be considered to have structural brain lesions and to require brain imaging studies .
 this is the first case of virus - associated encephalitis / encephalopathy in which the pathogen was hantaan virus . 
 a 53-yr - old man presented fever , renal failure and a hemorrhagic tendency and he was diagnosed with hemorrhagic fever with renal failure syndrome ( hfrs ) . in the course of his illness , mild neurologic symptoms such as dizziness and confusion developed and magnetic resonance images revealed a reversible lesion in the splenium of the corpus callosum . 
 this case suggests that hfrs patients with neurologic symptoms like dizziness and mental slowing should be considered to have structural brain lesions and to require brain imaging studies . 
INTRODUCTION
CASE REPORT
DISCUSSION