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Paper text:
a 52-year - old man was admitted after a 1-month history of general weakness which was aggravated three days before an emergency room visit .
an initial neurologic examination revealed disorientation of time , place , person , attention deficit , immediate memory disturbance , dysarthria , weakness of bilateral upper extremities with increased deep tendon reflex and right hemiparetic gate .
the blood work noted an elevated eosinophil count ( 5,500/l , 41% of whole white blood cells ) .
the patient 's clinical history and basic examinations did not lend a clue to any identifiable cause of hypereosinophilia , which includes parasitic infection , neoplasm , vasculitis or allergy . additionally , the patient had no prior clinical symptoms or signs suggesting the occurrence of churg - strauss syndrome , which includes sinusitis or asthma .
the cardiac enzymes were increased by 7.3 ng / ml of creatine kinase - mb and 4.78 ng / ml of troponin - i .
a diffusion - weighted brain mri revealed multiple acute infarcts in bilateral border zones , as well as randomly distributed cortices ( fig .
focal intracerebral hemorrhaging was noted on the left frontal white matter on t2-weighted and gradient echo images ( fig .
an mr angiography and conventional cerebral digital subtraction angiography did not show any evidence of arterial or venous sinus abnormalities ( fig .
1e - h ) . under the diagnosis of acute hypereosinophilic syndrome , treatment consisted of 60 mg / day of prednisolon and 100 mg / day of aspirin .
clinical improvement was noted on the third day of treatment and the patient was discharged after two weeks with a full recovery of his general condition and no neurologic deficit .
idiopathic hypereosinophilic syndrome is defined by 1 ) persistent eosinophilia of 1,500/l or greater for at least six months or death before six months with signs and symptoms of hypereosinophilic syndrome disease , 2 ) lack of evidence of parasitic , allergic , or other recognized causes of eosinophilia despite careful examination , and 3 ) signs and symptoms of organ system involvement ( 4 ) .
our patient did not fulfill one of these criteria due to an acutely manifested symptom .
though there was no recognized cause of eosinophilia , the diagnosis of our case would be acute hypereosinophilia rather than idiopathic eosinophilic syndrome . in our patient ,
the organ involvement of eosinophils resulted in cerebral infarcts , increased cardiac enzymes and multiple lung nodules .
the cerebral infarcts were noted at the vascular border zone as well as randomly distributed cortices .
the absence of prolonged systemic hypotension episodes and negative cerebral angiographic results may suggest distal arteriolar occlusion related to local thrombi or distant microemboli and spontaneous resolution . in a patient with hypereosinophilia
, the source of thromboembolism is known to be the eosinophilic involvement of cardiac endocardium and cerebral arteriolar endothelium , because activated eosinophils injure human endothelial cells by releasing a number of cytopathic substances such as major basic protein ( 2 ) .
major basic protein is a potent stimulator of platelet activation and aggregation which binds to thrombomodulin and reduces its ability to inhibit the clotting cascade ( 5 ) .
cardiac endothelial injury is often extensive and results in fibrosis and thrombosis of endocardial surfaces , though it may be clinically silent at the early stages of disease ( 6 ) .
elevated cardiac enzymes and mild left ventricular hypokinesia on the echocardiogram in our patient might be related to cardiac involvement of hypereosinophilia or coexisting ischemic heart disease . however , a specific diagnosis could not be made because further extensive cardiac examination was not available . in cerebral arteries ,
this was proved by a prior experimental report and was related to the size of the embolic particles ( 7 ) .
thus , as shown in our case , the cerebral infarctions are produced at the vascular border zone as well as randomly distributed cortices .
the main mechanism of eosinophilic toxicity to cerebral arteriolar endothelial cells was thought to be through the production of the tumor necrosis factor ( tnf)- mediated by an eosinophil cationic granular protein and resultant multiple arteriolar fibrinocruoric thrombi ( 8) . hypereosinophilia and its neurologic manifestations have been discussed in many previous reports .
however , no report of a case with focal intracerebral hemorrhaging and angiographic demonstration of an intact cerebral vasculature has been reported .
the focal intracerebral hemorrhaging in our patient was thought to be unusual because the individual infarct size was not large and no bleeding diathesis was observed .
this may suggest that there could be direct endothelial injury or vasculitis caused by eosinophilic infiltration as well as distant thromboembolism .
another possible mechanism of the border zone infarct is blood hyperviscosity with local thrombus formation .
both border zone infarcts in extreme hypereosinophilia , as well as hyperviscosity states from polycythemia vera have been reported ( 9 , 10 ) .
however , even in those cases , the cause of cerebral infarcts is more likely a microthromboembolism related to a prothrombotic state rather than local arterial thrombosis , unless the gross arterial or venous obstructions were demonstrated on angiograms ( 10 ) .
this case suggests that multiple cerebral infarcts in the vascular border zone without a specific recognizable cause , as well as cerebral angiographic abnormalities , can be a cause of neurologic manifestation associated with hypereosinophilia .
though the infarct sizes are not extensive , intracerebral hemorrhaging may be accompanied with infarcts related to hypereosinophilia .
we report a case of hypereosinophilia causing multiple areas of cerebral infarcts . a 52-year - old korean man presented with dysarthria and weakness in both arms . 
 a brain mri revealed multiple acute infarcts in the distal border zone with focal intracerebral hemorrhage , whereas a cerebral angiogram was not remarkable . 
 the eosinophil count was 5,500/l and was accompanied by elevated cardiac enzyme levels . 
 the pattern of cerebral infarcts and laboratory results suggest a thromboembolic infarction associated with hypereosinophilia .