Graefe's Arch Clin Exp Ophthalmol (1993) 231:711-717 Graefe's Archive forClinical and Experimental Ophthalmology © Springer-Verlag 1993 Optic nerve compression by carotid arteries in low-tension glaucoma Isaac Gutman 1, Shlomo Melamed 2, Isaac Ashkenazi 2 Michael Blumenthal 3 1 Goldschleger Eye Institute, Neuro-Ophthalmology Unit, Tel-Hashomer 52621, Israel z Goldschleger Eye Institute, Glaucoma Service Chaim Sheba Medical Center, Tel-Hashomer 52621, Israel 3 Sackler Faculty of Medicine, Chaim Sheba Medical Center, Tel-Hashomer 52621, Israel Received : 30 November 1991 / Accepted: 14 August 1992 Abstract. Low-tension glaucoma (LTG) is manifested by glaucomatous optic nerve damage and visual field loss despite normal intraocular pressure (IOP). We describe 62 patients with classical signs of LTG. Computed to- mography (CT) was performed in all patients. In 56 of the patients (90.3%), pathology of the intracavernous carotid arteries adjacent to the intracranial opening of the optic canal could be demonstrated. In 28 patients (45.2%) a clear asymmetry of the optic nerve cupping was found and could be correlated with the severity of the carotid artery pathology. A control group of 24 age- matched patients included five (20.8%) with intracaver- nous carotid artery calcification and only one (4.2%) with intracavernous ectasia. We suggest that calcifica- tion, dilatation and ectasia of the carotid artery into the optic canal may play an important role in the patho- genesis of many cases of LTG. The close proximity of the carotid artery to the optic nerve at this location may result in compressive neuropathy with subsequent glau- comatous damage of the optic nerve head. Introduction The term low-tension glaucoma (LTG) refers clinically to typical glaucomatous damage of the optic nerve head and visual field loss despite normal intraocular pressure (IOP) [10]. For many years, various investigators have commented on the differences in pathogenesis, clinical behavior and response to therapy between LTG and high-tension glaucoma (HTG) [1, 16]. Several factors believed to be associated with increased vulnerability of the optic nerve to normal IOP have been reported in LTG. These include reduction in systemic blood pressure [13], transient shock-like states caused by bleeding or myocardial infarction [8], atherosclerosis of the optic nerve vasculature [13], systemic tendency to arterial va- sospasm [9], pressure on the optic nerve from adjacent Correspondence to: I. Ashkenazi tumors [6] and congenital malformations of the optic nerve head [11]. We report here 62 patients with the clinical picture of LTG. In 56 patients (90.3%) computed tomography (CT) of the base of the skull revealed calcification and dilatation of the internal carotid arteries. We suggest that this may be an important contributing factor to the glaucomatous damage of the optic nerves and visual field changes in LTG. Materials and methods Sixty-two consecutive patients with LTG seen at the Goldschleger Eye Institute between 1985 and 1990 were included in this study. Thirty-three (53.2%) of them were male and 29 (46.8%) female. Their average age was 71.2_+8.4 years (range 51-92 years). The mean duration of follow-up was 4.34 ± 2.8 years (range 1-14 years). Demographic and clinical data are summarized in Table 1. Inclusion criteria were: (1) Glaucomatous changes in the optic nerve head, (2) characteristic visual field defects and (3) persistence of IOP greater than 20 mmHg without medical therapy, confirmed by normal diurnal curves. All patients were submitted to a complete ophthalmological and neuro-ophthalmological examination which included best cor- rected visual acuity, IOP measured by applanation tonometry, slit- lamp examination, gonioscopy, ophthalmoscopy, visual field anal- ysis (by computerized Goldman and tangent screen perimetry), (AOHRR) color vision test and pupil examinations. At the time of the neuro-ophthalmological evaluation none the patients were using antiglaucoma medications. Some subsequently received topical antiglaucoma treatment with no change of IOP. Table 1. Characteristics of the study population (n = 62) Characteristic Mean Range Age (years) 71.2 51-92 Follow-up (years) 4.3 1-14 Visual acuity 6/36 6/6-6/400 IOP (mmHg) 16.1 12-20 Cup/disc ratio 0.76 0.20-0.99 Color vision 2/6 0/6-6/6