Compressive Optic Neuropathy Workup

  • Author: Jonathan W Kim, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Oct 19, 2011
 

Laboratory Studies

  • Blood tests are sometimes helpful in the diagnosis of compressive optic neuropathy. However, the serologic workup should be guided by the history and clinical presentation.[6]
    • If thyroid ophthalmopathy is suspected, blood tests for thyroid function and anti-thyroid antibodies should be performed.
    • An elevated angiotensin-converting enzyme may be seen in sarcoidosis.
    • An elevated prostate specific antigen (PSA) may be helpful in male patients with suspected bony orbital metastases and optic nerve compression.
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Imaging Studies

Whenever there is clinical suspicion of compressive optic neuropathy (CON), a neuroimaging study is mandatory to determine the presence and location of the responsible lesion. With the sensitivity and specificity of modern neuroimaging, a negative scan essentially rules out the possibility of CON as the cause of vision loss.

In most cases of CON, magnetic resonance imaging (MRI) is the imaging modality of choice because of the excellent soft-tissue resolution of the anterior visual pathway and parasellar area; typically an orbit and brain MRI with and without contrast is ordered to evaluate a patient for CON.

MRIs are shown below.

Axial MRI taken 3 weeks after the onset of distortAxial MRI taken 3 weeks after the onset of distorted vision in the right eye; visual acuity is reduced to counting fingers at 1 ft. Evidence of optic nerve compression is not seen; disease in the sphenoid sinus is reported. MRI of same patient as in the image above taken 4 MRI of same patient as in the image above taken 4 months later. Patient responded well to IV Solu-Medrol, but symptoms returned when steroids were reduced. Large mass compressing the right optic nerve is seen. Biopsy revealed lymphoma. Neuroimaging study (MRI of brain and orbits) reveaNeuroimaging study (MRI of brain and orbits) revealed an extensive meningioma involving the left orbital apex (arrow).

Computed tomography (CT) scanning offers excellent visualization of the bony anatomy and is particularly useful to evaluate the intraconal space of the orbit. However, for imaging the orbital apex and optic canal, MRI is preferred over CT due to the absence of signal interference from adjacent bone seen on tomography.

Ultrasonography may be useful to document the presence of anterior orbital lesions but offers limited penetration into the deep orbit. However, in certain clinical situations, ultrasonography may be used to image patients quickly in the office in order to determine whether CT or MRI is warranted.

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Contributor Information and Disclosures
Author

Jonathan W Kim, MD  Director of Oculoplastic and Orbital Surgery, Co-director of Ocular Oncology Service, Co-director of Neuro-ophthalmology Service, Department of Ophthalmology, Stanford Medical Center

Jonathan W Kim, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Society of Ophthalmic Plastic and Reconstructive Surgery, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Coauthor(s)

Diana Katherine Lee  Fellow, Cancer Research Training Award; National Institutes of Health, National Cancer Institute

Disclosure: Nothing to disclose.

Talmadge (Ted) Cooper, MD  Adjunct Clinical Associate Professor, Department of Ophthalmology, Stanford Medical School

Talmadge (Ted) Cooper, MD is a member of the following medical societies: American Academy of Ophthalmology and American College of Medical Informatics

Disclosure: Nothing to disclose.

Specialty Editor Board

Edsel Ing, MD, FRCSC  Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Brian R Younge, MD  Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

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
  1. Miller NR, Newman NJ, Biousse V. Walsh and Hoyt's Clinical Neuro-Ophthalmology. 6th ed. Lippincott, Williams & Wilkins; 2004.

  2. Schiefer U, Wilhelm H, Hart W. Neuro-ophthalmic presentations of orbital disease. In: Clinical Neuro-Ophthalmology: A Practical Guide. Wien & New York: Springer; 2007.

  3. Bulters DO, Shenouda E, Evans BT, Mathad N, Lang DA. Visual recovery following optic nerve decompression for chronic compressive neuropathy. Acta Neurochir (Wien). Apr 2009;151(4):325-34. [Medline].

  4. Shields AJ, Shields CL, Scartozzi R. Survey of 1264 patients with orbital tumors and simulating lesions: the 2002 Montgomery Lecture, Part 1. Ophthalmology. 2004;111(5):997-1008. [Medline].

  5. Hodson KE, Bowman RJ, Mafwiri M, et al. Low folate status and indoor pollution are risk factors for endemic optic neuropathy in Tanzania. Br J Ophthalmol. Oct 2011;95(10):1361-4. [Medline].

  6. Lee AG, Chau FY, Golnik KC, Kardon RH, Wall M. The diagnostic yield of the evaluation for isolated unexplained optic atrophy. Ophthalmology. May 2005;112(5):757-9. [Medline].

  7. Spoor TC. Atlas of Oculoplastic and Orbital Surgery. Informa Healthcare; 2007.

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Axial MRI taken 3 weeks after the onset of distorted vision in the right eye; visual acuity is reduced to counting fingers at 1 ft. Evidence of optic nerve compression is not seen; disease in the sphenoid sinus is reported.
MRI of same patient as in the image above taken 4 months later. Patient responded well to IV Solu-Medrol, but symptoms returned when steroids were reduced. Large mass compressing the right optic nerve is seen. Biopsy revealed lymphoma.
A 72-year-old man with a moderate decrease in vision in the left eye (20/20 right, 20/25 left). Fundus examination revealed a normal right optic nerve.
Same patient as in image above of a 72-year-old man with a moderate decrease in vision in the left eye (20/20 right, 20/25 left). Fundus examination revealed an atrophic left optic nerve.
Neuroimaging study (MRI of brain and orbits) revealed an extensive meningioma involving the left orbital apex (arrow).
 
 
 
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