eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Low Tension

Author: Iqbal Ike K Ahmed, MD, FRCSC, Clinical Assistant Professor, Department of Ophthalmology, University of Utah
Coauthor(s): 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: Jun 22, 2006

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

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

Frequency

United States

Up to 15-25% of patients with POAG experience LTG. 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

An increased prevalence of LTG exists in Japan.

Mortality/Morbidity

Loss of peripheral vision is associated with LTG.

Race

An increased prevalence of LTG exists in Japan.

Sex

LTG is more common in females than in males.

Age

The mean age of patients with LTG is 60 years; they are older than patients with POAG.

Clinical

History

  • Ocular history
  • Steroid use
  • Trauma
  • Vasospasm
    • Raynaud syndrome
    • Migraines
  • Coagulopathies - Previous blood loss or shocklike episode
  • Systemic nocturnal hypotension (notably in older thin, Caucasian women)
  • Autoimmune disorders (Patients often have evidence of other autoimmune diseases.)
  • Systemic vascular disease
  • Thyroid disease - Increased incidence of thyroid disease in patients with LTG (6 out 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).
  • Rule out ocular hypertension and POAG.
  • Refractive error - Myopia
  • Cornea
    • Keratic precipitates indicating uveitis
    • Krukenberg spindle indicating pigment dispersion
  • Iris - Transillumination defects or pigment dusting indicating pigment dispersion
  • Anterior chamber
    • By definition, LTG 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
  • IOP
    • Perform diurnal curve (should be <22 mm Hg).
    • May be asymmetric
    • Higher IOP in left eye (related to blood flow from carotid arteries)
  • Myopic - Greatest risk of progression
  • Senile sclerotic - Older with vascular disease
  • Focal ischemic - May be younger
  • Optic disc in LTG 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
    • Disc hemorrhages
    • Acquired pit
  • Retina - Arteriosclerotic changes indicating vascular disease
  • Visual fields in LTG as compared to high-tension glaucoma (controversial)
    • Focal
    • Closer to fixation
    • Deeper
  • Blood pressure - Nocturnal hypotension
  • Carotid bruit indicating carotid insufficiency

Causes

LTG is associated with the following:

  • Migraine
  • Peripheral vasospasm, Raynaud syndrome
  • Autoimmune disorders
  • Systemic vascular disease (ie, atherosclerotic disease)
  • 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. 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].

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

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

  4. 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].

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

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

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Further Reading

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Keywords

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

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Contributor Information and Disclosures

Author

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.

Coauthor(s)

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: Nothing to disclose.

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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