cerebral hyperperfusion syndrome ( chs ) is a dangerous complications following carotid endarterectomy ( cea ) or carotid artery stenting ( cas)3,4,7,11 ) . chs following cea or cas is characterized by unilateral headache , seizure , focal neurologic defects , and intracerebral hemorrhage in most severe form6,9 ) . little is known about the exact cause of chs ; however , a deterioration in cerebrovascular autoregulation seems to increase regional cerebral blood and lead to chs1 ) . rate of occurrence of chs after cas is reported to be 0.4% to 3%1,8,9 ) . although there are a few reports of chs occurring from three weeks to four weeks after cea , a delay in onset of over one week is very rare6 ) . risk factors for chs are known diabetes mellitus , old age , recent contralateral cea , post - interventional hypertension , contralateral carotid occlusion , intra - interventional ischemia , and administration of anticoagulants or antiplatelet agents . we describe a case of delayed chs , presenting as status epilepticus , three weeks after cas in a high risk patient . a 67-year - old woman was admitted for evaluation of an incidental finding of carotid bruit on physical examination . she had been treated for hypertension and diabetes mellitus for 10 years . on admission , magnetic resonance imaging ( mri ) revealed multiple old infarctions in the bilateral parieto - occipital junctions and right internal border zone area . mr angiography revealed occlusion of the right proximal internal carotid artery ( ica ) , and severe stenosis of the left proximal ica and orifices of both vertebral arteries ( va ) . digital subtraction angiography demonstrated total occlusion of the right proximal ica , 73% stenosis of the left proximal ica and more than 70% stenosis of both va orifices ( fig . the patient was pre - treated with aspirin and clopidogrel for 5 days before undergoing stenting at the left proximal ica and right va orifices via a transfemoral approach under local anesthesia ( fig . anti - hypertensive drugs including a calcium channel blocker ( ccb ) were administered to maintain systolic blood pressure below 140 mm hg . three weeks after cas , the patient presented to the emergency room with generalized tonic - clonic seizure for 40 minutes and stuporous mentality . the withdrawal response in the right extremities was decreased , but there was hyper - reflexia in all the extremities , with pathologic plantar reflexes bilaterally . brain mri showed high signal intensities in the left hemispheric white matter on flair , without diffusion restriction , pointing to vasogenic edema ( fig . slower waves were recorded on the left than on the right hemisphere on electroencephalograms , and there was no epileptiform discharge . after administration of antiepileptics and antihypertensives , the deteriorated mentality recovered slowly and seizures ceased . the patient 's blood pressure was controlled by high dose intravenous labetalol and losartan / hydrochlorothiazide . follow - up mri of two weeks after chs showed resolution of the vasogenic edema ( fig . perfusion ct was performed at the time of symptom development and 24 days after chs , when the state of the chs had improved . it revealed a higher cerebral blood volume ( cbv ) in both hemispheres at the onset than 24 days after chs . blood pressure was normalized by the prescribed drugs and the seizure was stabilized with valproic acid and levetiracetam . there have been a few reports of chs after cea , but it has rarely been described after cas6 ) . the pathophysiology of chs after cas remains unclear , but there are several possible mechanisms . , transient bradycardia and hypotension due to damage to the carotid artery baroreceptor can often occur during cas , and can result in further ischemic injury to damaged brains9 ) . thirdly , systemic hypertension secondary to cas can result in intense cerebral blood flow1,6 ) . the most important issue in this case is differentiation between chs and seizure due to a periprocedural thromboembolism . we performed perfusion ct at the time of symptom development and 24 days after chs when the chs had improved . in the perfusion ct , greater cbv was observed in both hemispheres at the onset of the chs than 24 days after the chs . periprocedural thromboembolism is a common adverse effect of cas and a risk factor for chs . if the patient had presented with seizure due to a periprocedural embolism , the features of the perfusion ct scan might have been different . the most common post - ictal perfusion abnormality is decreased cerebral blood flow and cerebral blood volume2 ) . ct perfusion revealed a reduced time - to - peak and mean - transient - time and increased cerebral blood volume and cerebral blood flow in the chs10 ) . the perfusion ct scan was compatible with chs , and the patient had no neurological deficit or clinical symptoms related to the chs , based on the results of blood pressure measurements over the 2 weeks after the chs . although we did not perform a special evaluation , the possibility of a diagnosis of periprocedural thromboembolism or other adverse effect seemed to be low . also , the large lesion and generalized clinical symptoms were more likely to be related to chs than to a thromboembolism . in the present case , the occurrence of chs was associated with multiple risk factors including ipsilateral occlusion , contralateral stenosis , poor collateral circulation , old age , long - standing hypertension , and administration of antiplatelet agents9,13 ) . although the patient had potential risk factors for chs , the latter could have been due to some other mechanism . another might be associated with the unstable status of preprocedural cerebrovascular reactivity in patients with various predisposing factors11 ) , or the unknown status of postprocedural cerebrovascular autoregulation11 ) . this case suggests that we should take into careful consideration all periprocedural risk factors for chs . in addition , it suggests that delayed onset of chs may occasionally present with status epilepticus . after cas , clinicians should observe patients who have undergone cas and have high risk factors for at least two or three weeks .
cerebral hyperperfusion syndrome ( chs ) is increasingly recognized as an uncommon , but serious , complication subsequent to carotid artery stenting ( cas ) and carotid endarterectomy ( cea ) . 
 the onset of chs generally occurs within two weeks of cea and cas , and a delay in the onset of chs of over one week after cas is quite rare . 
 we describe a patient who developed chs three weeks after cas with status epilepticus .