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. 2014 Jan 28;7(4):995–999. doi: 10.3892/etm.2014.1508

Table I.

Clinical data of 12 patients with NGODC.

Case no. Gender Age (years) Diagnosis Eye Duration of diseasea Morphology of cupping BCVAb Visual field defect
1 F 41 Neuromyelitis optica OS 2 years Diffuse OD 0.2, OS
FC/20 cm
Central scotoma
2 M 18 LHON OU 2 years Diffuse OD 0.1, OS 0.05 Central scotoma
3 F 62 CLRAO, CRVO OD 10 months Diffuse OD 0.15, OS 0.25 Inferior defect
4 M 26 Pituitary adenoma OU 10 months Bilateral nasal (more serious OD) OD 0.8, OS 0.8 Bitemporal hemianopsia
5 F 31 Cerebral hemorrhage OU 13 months Temporal OS, nasal OD OD 1.0, OS 1.0 Bilateral homonymous hemianopia in the right side
6 M 55 Optic neuritis OD 1 year Diffuse OD 0.3 Diffuse defect
7 M 47 Optic neuritis OU 10 months Diffuse OD 1.0, OS 0.12 Diffuse defect OS, more serious superiorly. Superior defect OD
8 F 8 Optic neuritis OU 6 months Diffuse OD 0.8, OS 0.8 Diffuse defect, more serious peripherally
9 F 48 Optic neuritis OS 1 year Diffuse 0.1 Unknown
10 M 39 Pituitary adenoma OU 2 years Diffuse OD 1.2, OS
HM before eye
Diffuse defect OS
Nasal hemianopia OD
11 F 30 Optic nerve injury OU 2 years Diffuse NLP, OU Unavailable
12 M 63 CRAO OD 3 months Diffuse 0.1 Diffuse defect
a

Indicates the time period between the clinical discovery of ODC and onset of the disease.

b

Indicates BCVA post follow-up.

NGODC, nonglaucomatous optic disc cupping; F, female; M, male; LHON, Leber’s hereditary optic neuropathy; CLRAO, cilioretinal artery occlusion; CRVO, central retinal vein occlusion; CRAO, central retinal artery occlusion; OS, oculus sinister; OU, oculus uterque; OD, oculus dexter; FC, finger counting; HM, hand movement; NLP, no light perception; BCVA, best corrected visual acuity.