Most automated perimetry artifacts are associated with diffuse abnormalities in the visual field. Occasionally, isolated quadrant defects can be seen.1 We recently encountered a case in which an apparent nerve fiber bundle defect was caused by improper positioning of the lens holder.
A 36-year-old man was seen in the neuro-ophthalmology clinic with a complaint of a subacute decrease of visual acuity in his right eye of approximately 1 month's duration. He denied any associated eye pain and had no history suggestive of demyelinating disease or similar episodes.
Neuro-ophthalmologic examination demonstrated visual acuity of 20/50 OD and 20/20 OS. There was a mild dyschromatopsia in the right eye and a 0.3-log unit, relative, afferent pupillary defect in the right eye. The remainder of the examination showed no abnormalities, with healthy optic nerves, no disc edema, and a cup-disc ratio of 0.2 in each eye. Automated perimetry (Humphrey Visual Field Analyzer, Program 24-2, Allergan Inc, San Leandro, Calif) showed a mild cecocentral depression in the right eye. The left visual field had a dense scotoma that looked like an arcuate defect emanating inferiorly from the blind spot and disappearing at the vertical midline (Figure 1). A dense scotoma that appeared to be a nasal step was also present. The patient denied any visual symptoms in the left eye and the nerve fiber layer and optic disc showed no abnormalities.
Humphrey visual field (24-2) program of subject's asymptomatic left eye. Gray scale and probability plots suggest inferior arcuate defect and inferior nasal step; however, inspection of individual threshold values shows that points in the scotoma were not seen (threshold of 0 dB), while those adjacent to the scotoma had normal values for threshold.
Careful ophthalmic examination of the Humphrey 24-2 visual field of the left eye demonstrated that the involved points were not seen, even with the brightest target, and all adjacent points had a normal threshold. A diagnosis of optic neuritis in the right eye was made, and he was treated conservatively. In the absence of visual symptoms in the left eye, this field was thought to be artifactual, and no further workup was performed.
He returned for follow-up treatment 6 weeks later with marked visual acuity improvement in the right eye and no change in the left. Visual acuity had improved to 20/20 OD and remained 20/15 OS. The dyschromatopsia and pupillary abnormalities had disappeared. A second automated perimetry (Humphrey 24-2) showed a mild, residual, cecocentral depression in the right eye. The left eye's visual field showed no abnormalities (Figure 2).
Results of a second 24-2 Humphrey field test in the left eye showing resolution of the scotoma.
Refractive errors during automated perimetry are corrected by placing a trial lens in a lens holder and centering it in front of the patient's eye. In our case, the dense nature of the scotoma, combined with the lack of symptoms and spontaneous resolution in the left eye on repeated testing suggested an artifact of testing. Placing the lens holder just right of center instead of centering it would produce a scotoma from the left edge of the lens holder emanating from the blind spot. To test this hypothesis, I attempted to create a similar defect by positioning the lens holder to connect to his own blind spot. A similar inferior arcuate scotoma was produced (Figure 3). A nasal step was not present, but trigonometric calculations show that placing the lens holder 40 mm from the nodal point of the eye would place the right edge of the lens holder at the 27° nasal horizontal when the left edge was at the blind spot. The lens holder can be moved closer to or away from the eye and could easily have been at this distance during our patient's field.
An attempt to reproduce the left eye's field defect by positioning the left edge of the lens holder in the blind spot. The inferior arcuate defect is nearly identical to that shown in Figure 1. A nasal step could be created by moving the lens holder away from the patient's eye.
While it is plausible that an asymptomatic demyelinating optic neuropathy could have caused this visual field, we believe it is unlikely. The patient's lack of complaints and symptoms, the rapid and complete resolution of the defect, and the depth of the scotoma with no abnormalities at the adjacent points, all argue against a true optic neuropathy. In addition, the defect extends vertically from the blind spot and stops at the vertical midline, unlike the more typical rounded anatomy of a nerve fiber bundle defect. Ophthalmologists should be aware of the importance of centering the lens holder in the patient's visual field and keeping the lens holder close to the patient's eye. Artifacts caused by abnormal placement of the lens holder can simulate glaucomatous visual field defects.
This study was supported in part by a grant from Research to Prevent Blindness Inc, New York, NY.
The author has no proprietary interest in the Humphrey Visual Field Analyzer or any competing product.
Corresponding author: Sean P. Donahue, MD, PhD, 1215 21st Ave, S Eighth Floor, Vanderbilt Medical Center East, Nashville, TN 37232-8808 (e-mail: firstname.lastname@example.org).
Donahue SP. Lens Holder Artifact Simulating Glaucomatous Defect in Automated Perimetry. Arch Ophthalmol. 1998;116(12):1681-1683. doi: