The origin of these lesions is unclear, with some evidence supporting inflammation within the subarachnoid space; traumatic hemorrhage that leads to blockage of the venous drainage of the perineurium and epineurium, leading to hemosiderin deposition that can result in the development of these cysts; congenital diverticula from persistent embryonic fissures; or hydrostatic CSF pressures . It has also been suggested that the restricted communication with the CSF in the thecal sac results in a ball-valve mechanism that permits one-way entry of CSF into the cyst during systolic pulsations, with no exit during diastole .