there is general consensus that radiosurgery is a preferred option to surgical removal for the treatment of an arteriovenous malformation in the basal ganglia , thalamus , and other deep brain areas . this is because surgical removal of a deep seated avm is especially difficult , producing high mortality and morbidity rates.1)2)6)8 ) consequently , gamma - knife radiosurgery ( gkrs ) has been employed for patients with a deep seated avm . although rare , radiation - induced vasculopathy is one of the most serious complications after gkrs.3)10 ) the basal ganglia and thalamus are extremely sensitive to radiation , therefore , gkrs for a deep seated avm has increased risk of side effects during the latency period.9)14 ) complication of large intracranial arteries related to gkrs has occasionally been reported.4)11 ) however , to the best of our knowledge , radiation induced ischemic injury to small arteries has never been reported . we report two cases of basal ganglia infarction after gkrs for deep seated avm , which were located adjacent to the avm . we suggested that radiation injury to the lenticulostriate artery could be one possible cause of the infarctions . a 70-year - old male presented with an atypical headache for several months . there was no de finite history of underlying disease or medication such as hypertension and/or diabetes . magnetic resonance imaging ( mri ) and cerebral angiography showed a spetzler - martin grade 2 avm , and the radiosurgery - based avm score ( rbas ) was 1.53 , located in the right deep temporal lobe , adjacent to the basal ganglia ( fig 1a , b ) . it was also drained to the basal vein of rosenthal and straight sinus ( fig . gkrs was performed with a 9.6cc lesion volume and a 20 gy marginal dose ( fig . one year later , a post - radiosurgical mri follow - up showed nidus regression . seventeen months after the radiosurgery procedure , the patient presented with acute - onset left hemiparesis ( 4/5 ) and sensory change . mri showed an acute cerebral infarction at the right basal ganglia in the lenticulostriate artery territory , in an area adjacent to the gkrs ( fig . the patient was administered 100 mg of aspirin from the stroke onset , and suffered no additional ischemic attack . three months later , he recovered without prominent deficit ( modified rankin scale , mrs = 0 ) . it is interesting to note that complete obliteration of the avm was confirmed at the 2-year follow - up angiography ( fig . a 54-year - old male presented with an incidentally - detected avm during his health examination . mri and cerebral angiography showed a spetzler - martin grade 3 avm , and rbas score was 1.78 in the right basal ganglia ( fig . it was mainly supplied by the right m1 segment , and was drained into the internal cerebral vein ( fig . gkrs was performed with a 2.4 ml lesion volume and a 18 gy marginal dose ( fig . eleven months after gkrs , the patient presented with sudden - onset left hemiparesis ( 2/5 ) . subsequent mri showed an acute cerebral infarction in the right putamen , which probably originated by occlusion of the lateral lenticulostriate arteries ( fig . the patient suffered no additional stroke attack , he then recovered with slight disability ( mrs = 2 ) at 3 months from onset . remarkably , the draining vein had decreased in diameter and most of the arteriovenous shunt including the nidus was no longer visible ( fig . a 70-year - old male presented with an atypical headache for several months . there was no de finite history of underlying disease or medication such as hypertension and/or diabetes . magnetic resonance imaging ( mri ) and cerebral angiography showed a spetzler - martin grade 2 avm , and the radiosurgery - based avm score ( rbas ) was 1.53 , located in the right deep temporal lobe , adjacent to the basal ganglia ( fig 1a , b ) . it was also drained to the basal vein of rosenthal and straight sinus ( fig . gkrs was performed with a 9.6cc lesion volume and a 20 gy marginal dose ( fig . one year later , a post - radiosurgical mri follow - up showed nidus regression . seventeen months after the radiosurgery procedure , the patient presented with acute - onset left hemiparesis ( 4/5 ) and sensory change . mri showed an acute cerebral infarction at the right basal ganglia in the lenticulostriate artery territory , in an area adjacent to the gkrs ( fig . the patient was administered 100 mg of aspirin from the stroke onset , and suffered no additional ischemic attack . three months later , he recovered without prominent deficit ( modified rankin scale , mrs = 0 ) . it is interesting to note that complete obliteration of the avm was confirmed at the 2-year follow - up angiography ( fig . a 54-year - old male presented with an incidentally - detected avm during his health examination . mri and cerebral angiography showed a spetzler - martin grade 3 avm , and rbas score was 1.78 in the right basal ganglia ( fig . it was mainly supplied by the right m1 segment , and was drained into the internal cerebral vein ( fig . gkrs was performed with a 2.4 ml lesion volume and a 18 gy marginal dose ( fig . eleven months after gkrs , the patient presented with sudden - onset left hemiparesis ( 2/5 ) . subsequent mri showed an acute cerebral infarction in the right putamen , which probably originated by occlusion of the lateral lenticulostriate arteries ( fig . the patient suffered no additional stroke attack , he then recovered with slight disability ( mrs = 2 ) at 3 months from onset . remarkably , the draining vein had decreased in diameter and most of the arteriovenous shunt including the nidus was no longer visible ( fig . gkrs is an important therapeutic modality for a deeply located cerebral avm.6)8 ) at the expense of a latency period to cure of 2 - 3 years , successful angiographic obliteration of avms is generally seen in approximately 70% of cases following radiosurgical treatment.3)5 ) although gkrs is a widely accepted treatment modality , progressive intracranial artery occlusion due to radiation induced vasculopathy is a serious side effect of conventional radiation therapy for intracranial disease . as the follow - up lengthens in modern series , details of radiation - induced injury have become more clearly elucidated . because the basal ganglia and thalamus are extremely sensitive to radiation side effects and hemorrhage during the latency period , deep avms have increased risks associated with radiosurgical therapy.9)12 ) in addition , one autopsy study reported that a normal surrounding blood vessel may also be affected by irradiation of 10 gy or more , and remarkable intimal hypertrophy with fragmentation of the elastic laminae , or even complete occlusion , can occur in these arteries.13 ) vascular complication associated with gkrs for deep avm has been noted in several case reports , including de novo aneurysm formation , venous varix formation or stenosis of major intracranial arteries . there have been occasional reports of stenosis or occlusion of major cerebral arteries occurring several years after stereotactic radiosurgery for cerebral arteriovenous malformations.4)7)11 ) exposure of a major cerebral vessel to radiation doses of 15 to 25 gy can potentially result in postradiosurgical stenosis or occlusion , although the incidence occurs in fewer than 1% of patients.11 ) some literature studies have reported that steno - occlusive complication could occur even at larger intracranial arteries after gkrs , in spite of low - dose radiation exposure.7)12 ) however , in the current study , in both cases the ischemic injury involved small perforating arteries ( lateral lenticulostriate arteries ) , and those events occurred at 11 and 17 months after the gkrs . a limitation to this case report is that there might be some debate about the etiology , because we present only 2 case reports and both patients had other risk factors for acute stroke . the patient in case 1 was old ( 70-year - old ) , and the patient in case 2 had underlying hypertension . therefore , an alternative explanation of the underlying cause in each case may be a small vessel occlusion due to atherosclerosis . in addition , evidence of radiation induced vasculopathy has not been confirmed in our two cases . in this regard , future prospective studies and long - term follow - up are necessary to prove the relationship between delayed perilesional ischemic injury and gkrs for deep seated avms . the authors present two cases of delayed perilesional ischemic events after gkrs for a deep seated avm , which occurred at 11 and 17 months after the treatment and may have been caused by radiation injury to the lateral lenticulostriate arteries . although alternative causes of the ischemic events are possible , awareness of the possibility of radiation - induced vasculopathy of small arteries will be helpful in establishing early and accurate diagnoses along with the appropriate therapy . larger studies with longer , formal angiographic follow - up will be necessary to clarify these events and their clinical significance .