While it is recognised that glaucoma can cause diffuse, non-specific losses in sensitivity in the visual field (VF), specific localised losses in VF sensitivity are considered most useful diagnostically. Nasal step, arcuate and paracentral ‘nerve fibre bundle’ VF defects represent the characteristic pattern defects that occur in glaucoma 1, 2 and typically reflect the course of retinal nerve fibres respecting the nasal horizontal meridian. Commonly, glaucomatous VF loss occurs in the upper hemi-field and affects paracentral regions.3-5 In contrast, glaucomatous pattern VF defects that are temporal wedge in nature are much less common 6 and are arguably less well recognised as a result. In this short article we present the case of a patient with a temporal wedge VF defect due to glaucoma.
Initial presentation
A 66-year-old Caucasian woman initially presented to Manchester Royal Eye Hospital (MREH) in 2003, having been found during a routine sight test to have elevated intraocular pressures (IOPs) of 25mmHg in both eyes along with a suspiciously cupped optic disc. At the initial ophthalmology assessment, the patient was noted to be asymptomatic and had recently been diagnosed with diabetes mellitus. It had been when she attended for diabetic retinopathy screening that her community optometrist referred her for suspect glaucoma. There was no previous history of ocular disease and no family history of glaucoma.
On examination, the patient was noted to have normal visual acuities, modestly raised IOPs of 22mmHg in the right eye and 24mmHg in the left eye, modestly thicker than average central corneal thicknesses (~580 microns in each eye), a normal anterior segment with gonioscopically wide open angles, and a cup to disc ratio documented as ~0.7 in each eye, with inferior neuroretinal rim thinning, particularly in the right eye. Subsequent maximum IOPs were noted to be 27mmHg in the right eye and 28mmHg in the left eye. Full threshold 24-2 VF testing on the HFA revealed an abnormal glaucoma hemi-field test (GHT) in the right eye and a borderline GHT in the left eye. The patient was diagnosed with primary open-angle glaucoma and initially commenced on guttae latanoprost od nocte right and left. At first follow-up the patient was noted to have had a satisfactory response at 15mmHg in both eyes, and thereafter she continued to be monitored in the consultant led glaucoma service, with treatment subsequently being modified to dual therapy with guttae travaprost od nocte right and left and guttae dorzolamide bd right and left.
Follow-up
In 2010 the patient was transferred to the hospital’s Optometry Led Glaucoma Assessment (OLGA) clinic for monitoring while continuing the same treatment. On assessment, both optic discs showed large cup to disc ratios (RE ~0.85 LE ~0.80) with the right eye in particular showing both inferior and, significantly, nasal rim excavation (Figure 1).
[CaptionComponent="1039"][CaptionComponent="1040"]Visual fields on the HFA showed an abnormal GHT in the right eye and borderline GHT in the left eye (Figure 2).
[CaptionComponent="1041"]There is a consistent right eye temporal VF defect and variable companion superior/inferior sensitivity losses (with a possible intermittent nasal step loss) across VFs undertaken on the HFA from 2010 onwards (Figure 3).
[CaptionComponent="1042"]These right eye defects are consistent with a diagnosis of glaucoma, with an abnormal GHT and with at least three non-edge locations located within the superior/inferior hemi-field depressed to the 5 per cent probability level (P<0.05), and with at least one point depressed to the 1 per cent level (P<0.01) on the pattern deviation plot.7 Subsequent Goldmann VF testing (Figure 4) confirmed the presence of a temporal wedge loss of sensitivity in the right eye consistent with the nasal rim excavation present at the right optic disc.
[CaptionComponent="1043"]Temporal wedge
Damage to nerve fibres on the nasal side of the optic disc may result in temporal wedge-shaped VF defects. Occasionally, these defects are seen as the sole defect. Sometimes, as is the case here, there may be companion losses in sensitivity elsewhere in the VF. Temporal wedge defects may not necessarily respect the horizontal meridian, probably because the retinal nerve fibres ‘kink up’ at the retinal horizontal raphe. The more common pattern of temporal loss in sensitivity is inferiorly more than superiorly, as appears to be evidenced from the Goldmann plot in this case. Although temporal wedge VF defects are known to be a form of glaucomatous VF loss, these defects are much less prevalent 6 in comparison to arcuate and nasal step defects, and are arguably less well recognised as a result, sometimes not being specifically listed as a ‘textbook’ defect characteristic of glaucoma.1 Arcuate pattern loss and loss in the nasal horizontal meridian (nasal step) has been well described in pattern analyses of glaucomatous VF defects,8 with temporal pattern loss being rare. 6 Temporal VF loss does, however, has significant differential diagnostic implications, not least with respect to possible neuro-ophthalmological diagnoses9 and identification of vertically aligned VF defects, as opposed to the more likely glaucoma-related nerve fibre bundle VF defects that respect the horizontal midline, and is one key factor in assessing requirements for neuro-imaging.10 Furthermore, it is also important to note that a temporal wedge defect may also be attributed to other ocular causes, including ischaemic optic neuropathy (ION), a macular hole, a lesion in the nasal retina, and optic nerve drusen.11
Conclusion
This case serves as a reminder of the potential for temporal wedge VF loss in glaucoma with loss of nasal neuro-retinal rim. While superior, inferior and nasal loss of sensitivity is more common, this case highlights that glaucoma defects can occur anywhere in the VF.
References
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Dr Robert Harper is optometrist consultant at Manchester Royal Eye Hospital where Sonali Patel is a specialist optometrist at Oxford Eye Hospital