June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Cecocentral Scotoma: A Neuro-Ophthalmic Revisionist Approach
Author Affiliations & Notes
  • Steven A Newman
    Ophthalmology, University of Virginia, Charlottesville, VA
  • Footnotes
    Commercial Relationships Steven Newman, None
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Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2605. doi:https://doi.org/
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      Steven A Newman; Cecocentral Scotoma: A Neuro-Ophthalmic Revisionist Approach. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2605. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Although homonymous hemianopsia, bitemporal, and arcuate visual field defects are by far the most common, the most classic visual field defect in neuro-ophthalmology has been the central scotoma. Literature from the mid-20th century emphasized the unique nature of cecocentral scotomas seen in patients with toxic and nutritional pathology. The fact that macular pathology can produce central scotomas has also been recognized and the distinction between retinal and neuro-ophthalmic disease has proved to be a major clinical distinction.

Methods: A retrospective study of 193 patients referred to the Neuro-Ophthalmology Division at the University of Virginia and coded for central and cecocentral scotomas. Patterns were analyzed. Foveal sensitivity was available on all fields. Most patients were studied with a 10-2 program as well as a 24-2 program. Some patients were studied with a V size test object (dense defects or poor central vision).

Results: Twenty-nine charts were excluded for either transient central scotomas, or what appeared to be arcuate or paracentral defects. Fourteen charts were classified as unknown etiology. Of the remaining 150 patients, 80 had evidence of macular pathology, (67 having clear maculopathy and 13 with retinal vascular disease). Of those with primary optic nerve pathology, optic neuritis and compressive optic neuropathies (24 each) were the most common. This was followed by anterior ischemic optic neuropathy (17 cases), 2 patients with neuroretinitis, 2 patients with neuromyelitis optica, and 1 patient with traumatic optic neuropathy. The classical finding of central scotomas was seen in 2 cases of Leber’s, 1 case of dominant optic atrophy, 2 cases of nutritional optic neuropathy, and 1 case of toxic optic neuropathy.

Conclusions: In spite of a selective referral bias, retinal disease was the most common pathophysiology causing central and cecocentral scotomas. The addition of OCT and anatomic studies helped to distinguish these, although even when the macula looked normal, functional studies such as multifocal ERG may be necessary. The use of the 10-2 program and a V size test object is often necessary to recognize the pattern of field defect. Even classical, toxic, metabolic, and hereditary optic neuropathies may involve central fixation without extension to the blind spot.

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