eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Low Tension

Author: Jacqueline Freudenthal, MD, Co-Investigator, Ophthalmic Consultants Centre, Toronto
Coauthor(s): Iqbal Ike K Ahmed, MD, FRCSC, Clinical Assistant Professor, Department of Ophthalmology, University of Utah; Baseer U Khan, MD, Staff Physician, Department of Ophthalmology, University of Toronto, Canada; Khalid Hasanee, MD, Glaucoma and Anterior Segment Fellow, Department of Ophthalmology, University of Toronto
Contributor Information and Disclosures

Updated: Jan 29, 2010

Introduction

Background

Low-tension glaucoma (LTG) is a chronic optic neuropathy that affects adults. Its features parallel primary open-angle glaucoma (POAG), including characteristic optic disc cupping and visual-field loss, with the exception of a consistently normal intraocular pressure (IOP), ie, less than 22 mm Hg.

Pathophysiology

Low-tension glaucoma is an optic neuropathy with chronic loss of retinal ganglion cells (RGC) due to a genetic hypersensitivity to IOP. Low-tension glaucoma also is due to vascular factors, including vasospasm and ischemia.

Frequency

United States

Up to 15-25% of patients with POAG experience low-tension glaucoma. According to the Baltimore Eye Study, 50% of individuals with glaucomatous disc and visual-field changes had an IOP of less than 21 mm Hg on a single visit, and 33% had an IOP of less than 21 mm Hg on 2 measurements.

International

The prevalence of low-tension glaucoma is higher in Japan and Korea.1

Mortality/Morbidity

Loss of peripheral vision is associated with low-tension glaucoma.

Race

The prevalence of low-tension glaucoma is higher in Japan and Korea.1

Sex

Low-tension glaucoma is more common in females than in males.

Age

The mean age of patients with low-tension glaucoma is 60 years; they typically are older than patients with POAG.

Clinical

History

  • Ocular history
  • Steroid use
  • Trauma
  • Vasospasm 
  • Coagulopathies - Previous blood loss or shocklike episode
  • Systemic nocturnal hypotension (notably in older thin, white women)
  • Autoimmune disorders (evidence of other autoimmune diseases common)
  • Systemic vascular disease
  • Thyroid disease - Increased incidence of thyroid disease in patients with low-tension glaucoma (6 of 25 patients in 1 series)
  • Sleep apnea (particularly in heavy men)
  • Alzheimer disease - Associated with mild increase in cup-to-disc ratio
  • Family history of glaucoma or optic neuropathy

Physical

  • Conduct general medical examination (eg, blood pressure, carotid arteries).
  • Exclude ocular hypertension and POAG
  • Refractive error - Myopia
  • Cornea 
    • Central corneal thickness thinner in normal-tension glaucoma2 in correlation with severity
    • Keratic precipitates indicating uveitis
    • Krukenberg spindle indicating pigment dispersion
  • Iris - Transillumination defects or pigment dusting indicating pigment dispersion
  • Anterior chamber 
    • By definition, low-tension glaucoma has an open, normal-appearing angle.
    • Rule out angle closure and angle recession.
  • Lens - Glaucomflecken indicating previous IOP elevation, probably secondary to acute angle closure
  • Posterior synechiae
  • Peripheral anterior synechiae
  • Intraocular pressure 
    • Perform diurnal curve (should be <22 mm Hg).
    • May be asymmetric
    • Higher IOP in left eye (related to blood flow from carotid arteries) 
      • IOP fluctuation leads to greater visual-field progression in normal-tension glaucoma2
      • Other - Corneal compensated IOP using the Ocular Response Analyzer3
  • Myopic - Greatest risk of progression
  • Senile sclerotic - Older with vascular disease
  • Focal ischemic - May be younger
  • Optic disc in low-tension glaucoma as compared to high-tension glaucoma (controversial)
  • Larger discs
  • Peripapillary disc atrophy (particularly beta zone)
  • Thin disc rims; more commonly shows notching, more sloping of cup
  • Narrow vessels in peripapillary area, independent of stage of the disease4
  • Disc hemorrhages
  • Acquired pit
  • Retina - Arteriosclerotic changes indicating vascular disease
  • Visual fields in low-tension glaucoma as compared to high-tension glaucoma (controversial)
  • Focal
  • Closer to fixation
  • Deeper
  • Blood pressure - Nocturnal hypotension
  • Carotid bruit indicating carotid insufficiency

Causes

Low-tension glaucoma is associated with the following:

  • Migraine
  • Peripheral vasospasm, Raynaud syndrome
  • Generalized peripheral vascular endothelial dysfunction5  
  • Ocular circulation insufficiency (lower ocular pulse amplitude)5  
  • Increased resistance index in the central retinal artery (role in progression of visual field defect)6
  • Impaired vascular autoregulation (prolonged arteriovenous venous passage time in relation to ocular perfusion)7  
  • Autoimmune disorders
  • Systemic vascular disease (ie, atherosclerotic disease, cerebrovascular insufficiency)8
  • Systemic nocturnal hypotension
  • Sleep apnea (decreases oxygen saturation)

More on Glaucoma, Low Tension

Overview: Glaucoma, Low Tension
Differential Diagnoses & Workup: Glaucoma, Low Tension
Treatment & Medication: Glaucoma, Low Tension
Follow-up: Glaucoma, Low Tension
References
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References

  1. Kim KCY, Ahn AMD, Seong SGJ. Does redefining of high intraocular pressure (IOP) according to IOP distribution change prevalence of normal tension glaucoma in Korea? [abstract]. World Glaucoma Congress, 2009. Available at http://www.worldglaucoma.org/WGC2009/. Accessed July 24, 2009.

  2. Caprioli J, Coleman AL. Intraocular pressure fluctuation a risk factor for visual field progression at low intraocular pressures in the advanced glaucoma intervention study. Ophthalmology. Jul 2008;115(7):1123-1129.e3. [Medline].

  3. Paul T, Radcliffe N, Shimmio M. Reclassification of normal and high tension glaucoma eyes using corneal compensated IOP [abstract]. World Glaucoma Congress, 2009. Available at http://www.worldglaucoma.org/WGC2009/. Accessed July 28, 2009.

  4. Akopov E, Astakhov Y, Nefedova D. Retinal vessels calibrometry in normal pressure glaucoma evaluation [abstract]. World Glaucoma Congress, 2009. Available at http://www.worldglaucoma.org/WGC2009/. Accessed July 28, 2009.

  5. Su WW, Cheng ST, Hsu TS, Ho WJ. Abnormal flow-mediated vasodilation in normal-tension glaucoma using a noninvasive determination for peripheral endothelial dysfunction. Invest Ophthalmol Vis Sci. Aug 2006;47(8):3390-4. [Medline].

  6. Delaney Y, Walshe TE, O'Brien C. Vasospasm in glaucoma: clinical and laboratory aspects. Optom Vis Sci. Jul 2006;83(7):406-14. [Medline].

  7. Plange N, Kaup M, Remky A, Arend KO. Prolonged retinal arteriovenous passage time is correlated to ocular perfusion pressure in normal tension glaucoma. Graefes Arch Clin Exp Ophthalmol. Aug 2008;246(8):1147-52. [Medline].

  8. Harris A, Siesky B, Zarfati D, et al. Relationship of cerebral blood flow and central visual function in primary open-angle glaucoma. J Glaucoma. Jan 2007;16(1):159-63. [Medline].

  9. Chauhan BC, Mikelberg FS, Balaszi AG, LeBlanc RP, Lesk MR, Trope GE. Canadian Glaucoma Study: 2. risk factors for the progression of open-angle glaucoma. Arch Ophthalmol. Aug 2008;126(8):1030-6. [Medline]. [Full Text].

  10. Asano E, Mochizuki K, Sawada A, Nagasaka E, Kondo Y, Yamamoto T. Decreased nasal-temporal asymmetry of the second-order kernel response of multifocal electroretinograms in eyes with normal-tension glaucoma. Jpn J Ophthalmol. Sep-Oct 2007;51(5):379-89. [Medline].

  11. Michelson G, Waerntges S, Engelhorn T, Doerfler A. Reduced optic radiation volume measured by DTI is correlated by arterial hypertension in normal tension glaucoma [abstract]. World Glaucoma Congress, 2009. Available at http://www.worldglaucoma.org/WGC2009/. Accessed July 28,2009.

  12. [Guideline] Screening for glaucoma: recommendation statement. US Preventive Services Task Force. National Guideline Clearinghouse. Mar 2005.

  13. [Guideline] Primary open-angle glaucoma. American Academy of Ophthalmology. National Guideline Clearinghouse. 2005.

  14. [Guideline] Comprehensive adult eye and vision examination. American Optometric Association. National Guideline Clearinghouse. 2005.

  15. Orgul S, Zawinka C, Gugleta K, Flammer J. Therapeutic strategies for normal-tension glaucoma. Ophthalmologica. Nov-Dec 2005;219(6):317-23. [Medline].

  16. Cheng JW, Cai JP, Wei RL. Meta-analysis of medical intervention for normal tension glaucoma. Ophthalmology. Jul 2009;116(7):1243-9. [Medline].

  17. Netland PA, Chaturvedi N, Dreyer EB. Calcium channel blockers in the management of low-tension and open-angle glaucoma. Am J Ophthalmol. May 15 1993;115(5):608-13. [Medline].

  18. Takako Nakagami, Yoshio Yamazaki, Fukuko Hayamizu. Prognostic Factors for Progression of Visual Field Damage in Patients with Normal-Tension Glaucoma. Japanese Journal of Ophthalmology. January, 2006;Volume 50, Number 1:38-42.

  19. Abedin S, Simmons RJ, Grant WM. Progressive low-tension glaucoma: treatment to stop glaucomatous cupping and field loss when these progress despite normal intraocular pressure. Ophthalmology. Jan 1982;89(1):1-6. [Medline].

  20. Fraunfelder FT, Roy FH. Current Ocular Therapy. Philadelphia: WB Saunders; 2000:488-9.

  21. Hitchings RA. Low tension glaucoma--its place in modern glaucoma practice. Br J Ophthalmol. Aug 1992;76(8):494-6. [Medline].

  22. Kawabata K, Kimura T, Fujiki K, Murakami A. [Ocular pulse amplitude in patients with open-angle glaucoma, normal-tension glaucoma, and ocular hypertensionby dynamic observing tonometry]. Nippon Ganka Gakkai Zasshi. Dec 2007;111(12):946-52. [Medline].

  23. Stewart WC, Reid KK. Incidence of systemic and ocular disease that may mimic low-tension glaucoma. J Glaucoma. 1992;1:27-31.

  24. Werner E. Progressive normal-tension glaucoma. I. Analysis. J Glaucoma. Dec 1996;5(6):422-6. [Medline].

  25. ²Kurtz S, Haber I, Kesler A. Corneal Thickness Measurements in Normal-tension Glaucoma Workups: Is It Worth the Effort?. J Glaucoma. Apr 15 [Epub ahead of print] 2009.

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Further Reading

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Keywords

low-tension glaucoma, low tension glaucoma, LTG, low-pressure glaucoma, optic neuropathy, intraocular pressure, primary open-angle glaucoma, POAG

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Contributor Information and Disclosures

Author

Jacqueline Freudenthal, MD, Co-Investigator, Ophthalmic Consultants Centre, Toronto
Jacqueline Freudenthal, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, and Canadian Ophthalmological Society
Disclosure: Nothing to disclose.

Coauthor(s)

Iqbal Ike K Ahmed, MD, FRCSC, Clinical Assistant Professor, Department of Ophthalmology, University of Utah
Iqbal Ike K Ahmed, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Canadian Ophthalmological Society, and Ontario Medical Association
Disclosure: Nothing to disclose.

Baseer U Khan, MD, Staff Physician, Department of Ophthalmology, University of Toronto, Canada
Baseer U Khan, MD is a member of the following medical societies: Canadian Ophthalmological Society
Disclosure: Nothing to disclose.

Khalid Hasanee, MD, Glaucoma and Anterior Segment Fellow, Department of Ophthalmology, University of Toronto
Khalid Hasanee, MD is a member of the following medical societies: Canadian Medical Association, Canadian Ophthalmological Society, and Ontario Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Neil T Choplin, MD, Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences
Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Association for Research in Vision and Ophthalmology, and California Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

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, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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