Asymmetric Papilledema in Idiopathic Intracranial Hypertension

We found the article by Bidot et al (1) and Dr Killer's response letter (2) regarding astronauts very interesting and supportive of the concept that some forms of compartmentation may be involved in the etiology of asymmetric optic disc edema. Bidot et al propose that the narrower optic canal is associated with less disc edema because restricted cerebrospinal fluid (CSF) flow from the brain to the optic nerve (ON) sheath results in lower intraorbital CSF sheath pressure. In this scenario, compartmentation is believed to offer a protective effect. For this theory to hold true, there would have to be a sufficient narrowing and restriction through the optic canal so that the CSF flow into the ON sheath is severely restricted but return flow to the brain is not. This is in contrast to the larger optic canal side where the full force of increased CSF pressure from the brain would presumably be transmitted through the normal sized canal. This theory assumes that the CSF pressure within the orbital ON sheath on the “normal” side is equal to that of the brain CSF. Asymmetry of the optic canal certainly is a possible etiology for our astronauts' findings. Four of 7 long-duration astronauts with optic disc edema have displayed optic disc edema asymmetry. However, astronaut disc edema seems to have some unique findings (3). First, in those astronauts with optic disc edema asymmetry after long-duration space flight, the higher degree of disc edema has always been documented in the right eye. Of 4 astronauts with asymmetric disc edema after long-duration flights, 3 had Frisen Grade 1 right disc edema with a normal left disc as documented by retinal photography. One had highly asymmetric disc edema with Frisen Grade 3, right eye, and Grade 1, left eye. In contrast, Bidot et al found the higher grade disc edema on the right side in only 9 of 20 patients (45%). For the Bidot protective theory to hold true in astronauts, the optic canal would have to be consistently narrower on the left in each of these astronauts. Such a consistent anatomical finding in 4 astronauts would be unlikely. Second, in one previous astronaut case report, a normal opening pressure on lumbar puncture was documented after a mission in the presence of asymmetric disc edema (4). In this same astronaut, we documented unilateral loss of spontaneous venous pulsations in the same eye during space flight that continued to be absent 21 months after return to Earth (5). We also documented, with optical coherence tomography and retinal photography, an astronaut with persistent asymmetric disc edema (right > left) 6 months following his mission in the presence of lumbar puncture opening pressures of 22 cm and 16 cm H2O, performed at one week and one year post mission, respectively (personal communication A.G.L.). These reports suggest that perhaps a unilateral ON sheath compartmentation existed on return to Earth in the presence of intracranial CSF pressures that had returned to normal after the mission. Although optic canal asymmetry could create ON sheath pressure differences in conjunction with elevated CSF pressure, it would not account for continued disc edema asymmetry in the presence of normal postmission opening pressure measurements. We are in agreement with Dr Killer than an examination of optic canal size in astronauts would be very informative and may shed light on the etiology of optic disc edema asymmetry in astronauts. Because of a paucity of objective information, this is currently a very hypothetical area of study. It might be appropriate to measure optic canal size in astronauts who have displayed well-documented disc asymmetry on previous long-duration missions. We suspect that computed tomography scan may be the best technique to measure optic canal size. A comparison of each of these astronaut's canal sizes with their degree of disc edema may provide very useful information.