a 66-year - old japanese woman was referred to us with a 6-month history of decreased vision and metamorphopsia in the left eye . visual acuity was 20 / 16 for the right eye and 20 / 32 for the left eye .
fundus examination showed mild epiretinal membrane in the macula of the right eye , and an elevated , oval , 1-disc - diameter , reddish - orange lesion accompanied by serous detachment of the neurosensory retina in the macula of the left eye ( fig .
during the choroidal arteriolar filling phase of icg angiography ( hra2 ; heidelberg engineering , heidelberg , germany ) , branching vessels ( arterioles ) appeared in blocked fluorescence , and a few dilated choroidal venules with dye leakage manifested in the early choroidal venular filling phase ( fig .
the dye proceeded extremely slowly in the choroidal venules , leaking to form polypoidal vessels .
notably , the early choroidal venular filling phase revealed pulsatile movements as subtle rhythmic variations in the caliber of the choroidal venule at an a - v crossing ( fig . 1b , yellow arrowhead ) , where the venule ( fig .
her left eye was diagnosed as pcv and treated with photodynamic therapy using verteporfin ( visudyne ; novartis ag , basel , switzerland ) according to the standard protocol ( 698-nm laser system , 50 j / mm , 83-s exposure time , 2,650 m spot size ) . within 3 months after treatment ,
the reddish - orange lesion gradually decreased in size with complete disappearance of the retinal detachment ( fig .
the present findings support the hypothesis that pulsations in pcv might occur at a - v crossings or at a - v shunts , as discussed in our previous study .
importantly , the pulsations disappeared when dye leakage from the polypoidal vessel ceased after treatment , suggesting a relationship between venous pulsations and polypoidal vessel formation .
regarding venous pulsations , spontaneous venous pulsation ( svp ) is well known on the optic disc , where the central retinal vein and artery are fixed to the bundle of the lamina cribrosa by dense collagen and elastic tissues , resulting in the vessel lumen being narrow at this location , and accounting for the greater frequency of occlusion at or near this site .
svp is generally believed to be caused by the oscillation of intraocular pressure , which is transmitted to the intraocular central retinal vein across the vessel walls , during the cardiac cycle at a significantly higher level than the pressure in the retrolaminar portion of the central retinal vein .
this theory may also explain the mechanism of pulsation in our case : the venous pulsations may be caused by oscillations of intraocular pressure transmitted to the choroidal venule during the cardiac cycle when there is a significant difference in intravenous pressure between both sides of the a - v crossing .
the cause of the difference in intravenous pressure may be that the choroidal venule is made unusually narrow by the compression at the a - v crossing . in the retina
, branch retinal vein occlusion occurs at the a - v crossing portion , particularly in arteriolar sclerosis : a vein compressed by an artery is occluded , showing stasis and dilation in the portion proximal to the a - v crossing . in the present case , a similar mechanism might contribute to the venous stasis and the increase in intravenous pressure , resulting in dilation of the portion proximal to the a - v crossing , that is , the polypoidal vessel , although occlusion did not occur .
consequently , fluctuations in blood flow may occur at an a - v crossing , causing variations in the caliber of the venule .
previous clinicopathologic studies revealing a close relationship between pathologic polypoidal choroidal venules and arterioles support this possibility .
this study suggests that unusual compression at a - v crossings may make the venule polypoidal , and fluctuations of blood flow and pressure in the venule may cause pulsatile movements in the vessel wall .
further studies elucidating the relationships between pulsation , a - v crossings , and polypoidal vessels would be helpful in understanding the pathogenesis of the formation of polypoidal vessels .
 it has been reported that pulsations in abnormal vessels are observed on indocyanine green ( icg ) angiography in half of patients with polypoidal choroidal vasculopathy ( pcv ) , although the mechanism of the pulsation is unknown . in this study 
 , we report a case of pcv showing venous pulsations at an arterio - venous ( a - v ) crossing , and discuss a possible mechanism of polypoidal vessel formation and pulsations in pcv . a 66-year - old female presented with a reddish - orange elevated lesion and serous retinal detachment in the macula of her left eye , and 
 was diagnosed as pcv . 
 she was treated with photodynamic therapy ( pdt ) , and followed - up through routine examinations , including icg angiography . 
 icg angiography at presentation showed a branching vascular network and choroidal venules with dye leakage ( polypoidal vessels ) in the left eye . 
 pulsations , supposedly of venous origin , were observed at an a - v crossing in the abnormal vessels . within 3 months after pdt , 
 the polypoidal vessel ceased to leak and the pulsations vanished . 
 the reddish - orange lesion gradually decreased in size with complete disappearance of retinal detachment . 
 this study suggests that an unusual compression at an a - v crossing may make a venule polypoidal , and fluctuations of blood flow and pressure in the venule may cause pulsatile movements of the vessel wall . 
Case Report
Discussion