Glaucoma, Low Tension Workup

  • Author: Jacqueline Freudenthal, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 29, 2010
 

Laboratory Studies

  • Blood tests in low-tension glaucoma (LTG)
    • Order a CBC count to rule out anemia.
    • Erythrocyte sedimentation rate (ESR) rarely is elevated in low-tension glaucoma and typically is obtained in cases of decreased central acuity with a pale nerve to rule out anterior ischemic optic neuropathy (AION).
    • Order rapid plasma reagent (RPR) and fluorescein treponema antibody (FTA) testing.
    • Checking for the presence of antinuclear antibody (ANA) is recommended to rule out collagen-vascular and autoimmune diseases. Screening for extractable nuclear antigens (ie, Ro, La, Sm) also is recommended to rule out autoimmune diseases.
    • Serum immunofixation for monoclonal gammopathy is indicated. Approximately 10% of patients with low-tension glaucoma have monoclonal gammopathy (paraproteinemia), which represents a benign condition two thirds of the time. However, lymphoproliferative disorders (ie, cancers) need to be ruled out by a hemato-oncology specialist if results from this test are positive.
    • High-sensitivity C-reactive protein is becoming the criterion standard for documenting both symptomatic and nonsymptomatic ischemic heart disease, and results often are positive in patients with low-tension glaucoma.
    • Mitochondrial testing for Leber should be ordered, when indicated.
    • Anticardiolipin antibody (ACA) testing should be performed, and an increased level is considered a risk factor for visual-field defect progression.[9]
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Imaging Studies

  • Optic nerve head and/or retinal nerve fiber analysis may be helpful in diagnosing and monitoring progression of glaucomatous optic neuropathy.
    • Analyze optic nerve head with confocal scanning laser ophthalmoscopy (SLO), eg, Heidelberg Retinal Tomograph, or optical coherence topography (OCT).
    • Analyze retinal nerve fiber with confocal SLO, OCT, or scanning laser polarimetry (GDx). Often, retinal nerve fiber layer changes may occur before any changes on visual-field testing. Most often, nerve fiber layer thinning occurs first in the superior and inferior poles.
  • Neuroimaging of orbits and head
    • MRI is the preferred imaging modality compared with CT scanning because of its higher sensitivity.
    • Controversy exists as to whether neuroimaging should be performed routinely. Some advocate referral to a neurophthalmologist if concerned.
    • Neuroimaging should be performed in any patient with the following:
      • Markedly asymmetric disease
      • Increased optic disc pallor relative to cupping
      • Unusual visual-field defects, particularly those with respect to the vertical midline
      • Rapid progression of visual fields
      • Rapid progression of optic neuropathies
      • Dyschromatopsia
      • Afferent papillary defect with mild cupping
  • If indicated, carotid Doppler testing is recommended to rule out carotid insufficiency.
  • When indicated, chest radiography is necessary to rule out sarcoidosis.
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Other Tests

  • To rule out nocturnal hypotension, 24-hour ambulatory blood pressure monitoring is advised.
  • The diurnal tension curve may need to be determined. Although IOP may be normal during an examination, the patient may have intermittent spikes in IOP throughout the day that may explain optic nerve and visual field damage.
  • Multifocal electroretinograms (mfERGs) provides an index of identification for a glaucomatous optic neuropathy in normal-tension glaucoma.[10]
  • Future diagnostic modalities - Ocular blood flow analysis
    • Scanning laser ophthalmoscopy - Retinal and choroidal, superficial optic nerve head
    • Doppler ultrasonography - Carotid arteries
    • Confocal scanning laser Doppler flowmetry (Heidelberg Retinal Flowmetry) - Short posterior ciliary artery circulation, optic nerve head
    • Diffuse tension MRI (DTI) - Reduction of the optic radiation volume in patients with normal-tension glaucoma, in relation to arterial hypertension and cerebral microangiopathy stage[11]
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Histologic Findings

  • Findings include posterior deformation of the cribriform plate, with compression of the lamina due to direct deformation by secondary vascular compression, resulting in glial atrophy.
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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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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: Nothing to disclose.

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.

References

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  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].

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  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/WGC/WGC2009/index.php. Accessed July 28,2009.

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