Asymmetric Papilledema in Idiopathic Intracranial Hypertension
Hanspeter E. Killer
Abstract
Hanspeter E. Killer
Abstract
We would like to congratulate Bidot et al (1) for their article on asymmetric papilledema. Their study is the first to demonstrate a morphological difference in the diameter of the optic canals in patients with asymmetric papilledema. The optic canal consists of 2 components: bone and meningothelial cells (2). Although bone is rigid, the meningothelial cells of the pia-arachnoid react to a variety of biological and mechanical stimuli (3,4). For example, increased intracranial pressure (ICP) causes proliferation of the number of meningothelial cells as well as an increase in their size (4). This, in turn, can result in thickening of the meningothelial cell layer, leading to narrowing of the subarachnoid space (SAS) surrounding the optic nerve and, eventually, to optic nerve compartmentation, perhaps protecting the optic nerve from the effects of increased ICP. This process has been demonstrated in an animal model (5) as well as in patients with papilledema who have undergone computed tomographic cisternography before and after intrathecal (spinal) injection of iodinated contrast material (6,7). In these patients, there is a decreased gradient of contrast between the lumbar SAS and the SAS surrounding the optic nerve (7). It would be interesting to see whether the Frisén grade of papilledema correlates with the contrast gradient. A further interesting aspect of the work by Bidot et al is that the visual field in the eye with the larger optic canal was more affected, although visual acuity was the same in both eyes. This finding also suggests that compartmentation might offer at least a temporary protective effect on the optic nerve; however, the effect of chronic compartmentation on cerebrospinal fluid circulation needs to be studied further. In addition to patients with increased ICP and papilledema, it might be worthwhile assessing the diameters of the optic canals in astronauts in whom optic disc swelling has developed during prolonged spaceflight (8) and comparing them with the optic canals of astronauts who never developed optic disc swelling. If the size of the optic canal is a major determinant of whether or not an individual develops optic disc swelling from increased ICP or another cause, one would expect that astronauts in whom disc swelling has been observed should have larger canals than those in whom optic disc swelling has not developed. In the meantime, we agree with Bidot et al that asymmetry of the diameter of the bony optic canal may produce a compartmentation phenomenon that protects the optic nerve from the effects of increased ICP and would add that it is possible that an increase in the thickness of meningothelial cell layer caused by a reaction to increased ICP may play a role as well, both in this setting and possibly in other optic nerve disorders (9).
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We would like to congratulate Bidot et al (1) for their article on asymmetric papilledema. Their study is the first to demonstrate a morphological difference in the diameter of the optic canals in patients with asymmetric papilledema. The optic canal consists of 2 components: bone and meningothelial cells (2). Although bone is rigid, the meningothelial cells of the pia-arachnoid react to a variety of biological and mechanical stimuli (3,4). For example, increased intracranial pressure (ICP) causes proliferation of the number of meningothelial cells as well as an increase in their size (4). This, in turn, can result in thickening of the meningothelial cell layer, leading to narrowing of the subarachnoid space (SAS) surrounding the optic nerve and, eventually, to optic nerve compartmentation, perhaps protecting the optic nerve from the effects of increased ICP. This process has been demonstrated in an animal model (5) as well as in patients with papilledema who have undergone computed tomographic cisternography before and after intrathecal (spinal) injection of iodinated contrast material (6,7). In these patients, there is a decreased gradient of contrast between the lumbar SAS and the SAS surrounding the optic nerve (7). It would be interesting to see whether the Frisén grade of papilledema correlates with the contrast gradient. A further interesting aspect of the work by Bidot et al is that the visual field in the eye with the larger optic canal was more affected, although visual acuity was the same in both eyes. This finding also suggests that compartmentation might offer at least a temporary protective effect on the optic nerve; however, the effect of chronic compartmentation on cerebrospinal fluid circulation needs to be studied further. In addition to patients with increased ICP and papilledema, it might be worthwhile assessing the diameters of the optic canals in astronauts in whom optic disc swelling has developed during prolonged spaceflight (8) and comparing them with the optic canals of astronauts who never developed optic disc swelling. If the size of the optic canal is a major determinant of whether or not an individual develops optic disc swelling from increased ICP or another cause, one would expect that astronauts in whom disc swelling has been observed should have larger canals than those in whom optic disc swelling has not developed. In the meantime, we agree with Bidot et al that asymmetry of the diameter of the bony optic canal may produce a compartmentation phenomenon that protects the optic nerve from the effects of increased ICP and would add that it is possible that an increase in the thickness of meningothelial cell layer caused by a reaction to increased ICP may play a role as well, both in this setting and possibly in other optic nerve disorders (9).
Key concepts: Papilledema, Optic nerve, Subarachnoid space, Medicine, Intracranial pressure, Visual acuity, Contrast (vision), Ophthalmology