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 .