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I enjoyed the recent study by Ogata et al, in which they attempted to assess the interrelation between intracranial vascular compression of the optic nerves and normal tension glaucoma.1 Coronal magnetic resonance images of the optic nerves were used to assess the degree of compression of the intracranial optic nerves and the supraclinoid internal carotid arteries. Compression of an optic nerve by a normal internal carotid artery was found in 51 of 103 eyes (49.5%) of patients with normal tension glaucoma and in 36 of 104 (34.6%) eyes of control patients. The degree of compression was noted to be greater in patients with normal tension glaucoma. These findings led the authors to conclude that one cause of normal tension glaucoma may be compression of the optic nerve by the internal carotid artery.
As noted in the discussion, Jacobson et al found compression of the intracranial optic nerve by the internal carotid artery to be common in asymptomatic patients (bilateral contact in 70%, bilateral compression in 12%, unilateral contact or compression in 5%).2 In symptomatic patients, Jacobson noted glaucomatous visual field defects and “saucer-like temporal excavation” of the optic disc on the side of the compression.3 Symptomatic patients also had temporal neuroretinal rim pallor and other signs of compressive optic neuropathy such as decreased visual acuity and decreased colour vision, thereby distinguishing them from patients with normal tension glaucoma.4
In the Ogata study, inclusion of three additional outcome measures would be useful in defining any association that may exist between intracranial optic nerve compression and pseudoglaucomatous cupping. Firstly, did patients with normal tension glaucoma and intracranial optic nerve compression have decreased visual acuity, decreased colour vision, or associated pallor of the temporal neuroretinal rim on the side of the compressed optic nerve? Secondly, was the observed cupping in eyes with normal tension glaucoma and optic nerve compression vertical in orientation (that is, pseudoglaucomatous) or horizontal or round (that is, non-glaucomatous), and did this configuration differ in eyes without optic nerve compression? Finally, was the diagnosis of normal tension glaucoma confined to the involved side in the nine patients with unilateral optic nerve compression, as the study hypothesis would predict?