Unilateral Glaucoma
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While any type of glaucoma can be unilateral, primary open-angle glaucoma, primary angle-closure glaucoma, primary infantile glaucoma, juvenile-onset glaucoma, and pigmentary glaucoma are generally bilateral diseases, the severity of which may be asymmetric in the two eyes.
This article reviews glaucoma associated with increased episcleral venous pressure (EVP) and glaucoma associated with iridocorneal endothelial (ICE) syndrome.
Several etiologies of unilateral glaucoma are discussed in detail in other articles, including Glaucoma, Pseudoexfoliation; Glaucoma, Uveitic; Glaucoma, Lens-Particle; Glaucoma, Drug-Induced; Glaucoma, Neovascular; Glaucoma, Intraocular Tumors; Glaucoma, Hyphema; Glaucoma, Angle Recession; and Glaucoma, Malignant.
In the early 1900s, Lauber provided histological evidence that the canal of Schlemm was connected to the episcleral venous network. Aqueous humor drains via the anterior surface of the ciliary body or through the trabecular meshwork, Schlemm canal, collector channels, and, subsequently, aqueous veins. These pathways have been termed unconventional and conventional, respectively.
While the unconventional pathway is independent of pressure, outflow via the conventional route is passive and depends largely on the difference between the intraocular pressure (IOP) and EVP; as EVP increases relative to IOP, or as resistance increases, flow decreases.
The 3 general pathophysiological mechanisms of increased EVP are arteriovenous anomalies, venous obstruction, and idiopathic. Arteriovenous anomalies associated with increased EVP include carotid-cavernous sinus fistula, orbital varix, Sturge-Weber syndrome, orbital-meningeal shunts, carotid-jugular venous shunts, and intraocular vascular shunts. Venous obstruction may be caused by a retrobulbar tumor, thyroid ophthalmopathy, superior vena cava syndrome, congestive heart failure, thrombosis of the cavernous sinus or orbital vein, vasculitis involving the episcleral or orbital vein, and jugular vein obstruction.
The pathophysiological mechanism underlying ICE syndrome remains unknown. However, the finding of chronic inflammatory cells in the corneal specimens of patients with ICE syndrome suggests a viral etiology. In a study using polymerase chain reaction techniques, 16 of 25 corneas from patients with ICE syndrome and 4 of 6 patients with herpetic keratitis were positive for herpes simplex virus.
Glaucoma associated with ICE syndrome is believed to be due to trabecular meshwork obstruction caused by peripheral anterior synechiae or, less commonly, an abnormal cellular membrane.
United States
The frequency of glaucoma associated with increased EVP or with ICE syndrome is unknown.
Glaucoma has been reported to occur in 30% of patients with Sturge-Weber syndrome, 5% of patients with thyroid ophthalmopathy, 11.6% of patients with scleritis, and 4% of patients with episcleritis.
Glaucoma is the third leading cause of blindness in the United States.
Because glaucoma may progress insidiously without causing symptoms, progressive glaucomatous damage may occur without the patient even being aware of the diagnosis.
Prompt and continued control of IOP can prevent ocular damage due to glaucoma.
Traumatic carotid-cavernous sinus fistulae occur more commonly in males than in females.
ICE syndrome occurs more commonly in females than in males.
Spontaneous carotid-cavernous sinus fistulae typically occur in middle-aged to elderly individuals, while traumatic carotid-cavernous sinus fistulae occur most commonly in young persons.
It has been reported that 60% of patients with glaucoma associated with Sturge-Weber syndrome acquire glaucoma before age 2 years, and the remaining patients develop glaucoma later in childhood or in early adulthood.
The onset of ICE syndrome generally occurs in early to middle adulthood.
Mansouri K, Sommerhalder J, Shaarawy T. Prospective comparison of ultrasound biomicroscopy and anterior segment optical coherence tomography for evaluation of anterior chamber dimensions in European eyes with primary angle closure. Eye. 2009 May 15. [Medline].
Kitsos G, Zikou AK, Bagli E, Kosta P, Argyropoulou MI. Conventional MRI and magnetization transfer imaging of the brain and optic pathway in primary open-angle glaucoma. Br J Radiol. 2009 May 11. [Medline].
Wittström E, Ponjavic V, Lövestam-Adrian M, Larsson J, Andréasson S. Electrophysiological evaluation and visual outcome in patients with central retinal vein occlusion, primary open-angle glaucoma and neovascular glaucoma. Acta Ophthalmol. 2009 Apr 27. [Medline].
Gandolfi SA, Cimino L, Sangermani C, et al. Improvement of spatial contrast sensitivity threshold after surgical reduction of intraocular pressure in unilateral high-tension glaucoma. Invest Ophthalmol Vis Sci. 2005 Jan. 46(1):197-201. [Medline].
Jain SS, Rao P, Kothari K, et al. Posterior scleritis presenting as unilateral secondary angle-closure glaucoma. Indian J Ophthalmol. 2004 Sep. 52(3):241-4. [Medline].
Kirsch M, Henkes H, Liebig T, et al. Endovascular management of dural carotid-cavernous sinus fistulas in 141 patients. Neuroradiology. 2006 Jul. 48(7):486-90. [Medline].
Spiegel D, Wetzel W, Neuhann T, Stuermer J, Hoeh H, Garcia-Feijoo J, et al. Coexistent primary open-angle glaucoma and cataract: Interim analysis of a trabecular micro-bypass stent and concurrent cataract surgery. Eur J Ophthalmol. 2009 May-Jun. 19(3):393-9. [Medline].
Peeters A, Webers CA, Prins MH, Zeegers MP, Hendrikse F, Schouten JS. Quantifying the effect of intraocular pressure reduction on the occurrence of glaucoma. Acta Ophthalmol. 2009 Apr 27. [Medline].
Albert DM, Jakobiec FA, Azar DT. Glaucoma associated with increased episcleral venous pressure. Principles and Practice of Ophthalmology. 2nd ed. WB Saunders Co; 2000. 2781-2792.
Alvarado JA, Underwood JL, Green WR, et al. Detection of herpes simplex viral DNA in the iridocorneal endothelial syndrome. Arch Ophthalmol. 1994 Dec. 112(12):1601-9. [Medline].
Cibis GW, Tripathi RC, Tripathi BJ. Glaucoma in Sturge-Weber syndrome. Ophthalmology. 1984 Sep. 91(9):1061-71. [Medline].
Font RL, Ferry AP. The phakomatoses. Int Ophthalmol Clin. 1972. 12(1):1-50. [Medline].
Manor RS, Kurz O, Lewitus Z. Intraocular pressure in endocrinological patients with exophthalmos. Ophthalmologica. 1974. 168(4):241-52. [Medline].
Uram M, Zubillaga C. The cutaneous manifestations of Sturge-Weber syndrome. J Clin Neuroophthalmol. 1982 Dec. 2(4):245-8. [Medline].
Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. 1976 Mar. 60(3):163-91. [Medline].
Weiss DI. Dual origin of glaucoma in encephalotrigeminal haemangiomatosis. Trans Ophthalmol Soc U K. 1973. 93(0):477-93. [Medline].
Suh MH, Yoo BW, Park KH, Kim H, Kim HC. Reproducibility of spectral-domain optical coherence tomography RNFL map for glaucomatous and fellow normal eyes in unilateral glaucoma. J Glaucoma. 2015 Mar. 24 (3):238-44. [Medline].
Ingrid U Scott, MD, MPH Jack and Nancy Turner Professor of Ophthalmology, Professor of Public Health Sciences, Penn State Eye Center, Pennsylvania State University College of Medicine
Ingrid U Scott, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Macula Society, Phi Beta Kappa, Retina Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience
Disclosure: Nothing to disclose.
Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
Bradford Shingleton, MD Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary
Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology
Disclosure: Nothing to disclose.
Unilateral Glaucoma
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