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Year : 2017  |  Volume : 20  |  Issue : 2  |  Page : 149-154

Retroprospective analysis of types of visual field defects (Octopus 900 perimeter-based study) at Shimla Hills

Department of Ophthalmology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India

Date of Web Publication14-Nov-2017

Correspondence Address:
Kalpana Sharma
Department of Ophthalmology, Indira Gandhi Medical College, Shimla - 171 001, Himachal Pradesh
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DOI: 10.4103/tjmr.tjmr_56_16

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Aim: This study aims to study the types of visual field defects (VFDs) among the patients who underwent automated perimetry. Subjects and Methods: This study was the analysis of VFs of the patients who underwent VF recording on Octopus 900 perimeter (HAAG-STREIT, AG, Switzerland) at Shimla hills (IGMC, Himachal Pradesh, India) situated at the height of 7 200 feet above sea level. Results: Among the most common causes of VFDs in glaucoma (n = 119) the most common VFD was paracentral scotoma (44.4%) followed by arcuate scotoma (23.42%). The next common cause leading to VFD was nonocular neurological (n = 33) in which the most common VFD was quadrantanopia (27%) followed by bilateral temporal hemianopia (18%). Other ocular causes of VFD were cataract, age-related macular degeneration, central retinal vein occlusion, branch retinal vein occlusion, diabetic retinopathy (DR), anterior ischemic optic neuropathy, retinitis pigmentosa, and optic neuritis. Conclusion: This study concludes that the most of the patients for whom perimetry was performed on Octopus 900 perimeter under ocular conditions, the glaucoma was the most common disease. The second most common cause of VFD was neurological, the common lesions being head trauma, cerebrovascular accidents (CVA), and pituitary adenomas. Therefore, the stimulus for this work was not only ophthalmological but also neurological. Therefore, VF measurement is critical component in diagnosing not only glaucomatous VFD but also other nonocular and ocular blinding conditions.

Keywords: Glaucoma, neurological causes, Octopus 900, perimetry

How to cite this article:
Sharma K, Sharma RL, Chaudhary KP, Gupta RK. Retroprospective analysis of types of visual field defects (Octopus 900 perimeter-based study) at Shimla Hills. Trop J Med Res 2017;20:149-54

How to cite this URL:
Sharma K, Sharma RL, Chaudhary KP, Gupta RK. Retroprospective analysis of types of visual field defects (Octopus 900 perimeter-based study) at Shimla Hills. Trop J Med Res [serial online] 2017 [cited 2020 Sep 23];20:149-54. Available from: http://www.tjmrjournal.org/text.asp?2017/20/2/149/218220

  Introduction Top

Perimetry is used extensively in diagnosis and follow-up of several eye diseases such as in glaucoma, diseases of retina and neurological diseases. The use in glaucoma is often discussed and well understood, however, it has various other applications that render it very useful in disease management and blindness prevention. These include the detection and/or management of conditions such as intraorbital lesions, papilledema, retinitis pigmentosa (RP), cranial tumors, and others.

  Subjects and Methods Top

All authors declare that consent was obtained from approved person for the publication of this article and accompanying images. All authors hereby declare that all experiments have been examined and approved by the IGMC Shimla hospital and have therefore been performed in accordance with the ethical standards laid down in the 2008 Declaration of Helsinki.

In this study, the VFs of the patients were recorded on Octopus 900 perimeter (HAAG-STREIT AG Switzerland) in our institution. It included all the reliable (Reliability factor <15) VFs. Unreliable VFs were excluded from the study which comprised: False positive catch trials more than 15%, false negative catch trials more than 15%. Reliability factor value more than 15.

The standard octopus examination parameters

The standard octopus examination parameters included background luminance of 1.27 cd/m2 (4asb), background color white, stimulus size of 0.430 diameter, stimulus color of white, and exposure of 100 ms. The VFs were analyzed according to following criteria: Morales et al.[1] stated octopus criteria for visual field defects (VFDs) as MD (mean deviation) >2 dB, loss of variance (LV) >6 dB, and at least seven points with sensitivity decreased >5 dB, three of them being contiguous. VF severity grading was done according to classification proposed by Mills et al.[2] according to Thomas et al.[3] field defects in neurological lesions, patients were classified into quadrantanopia and hemianopia; quadrantanopia was diagnosed if either of the following criteria were fulfilled. (1) Depression of thresholds 5 dB or more, in 3 or more contiguous points adjacent to the vertical meridian in the involved quadrant as compared to their mirror image points across the vertical meridian. (2) The corrected probability plot showed 3 or more points adjacent to the vertical meridian in the involved quadrant depressed to the 1% probability level with normal mirror image points across the vertical meridian. For the diagnosis of hemianopia, the diagnostic criteria for quadrantanopia had to be applicable to both quadrants comprising the hemifield.

Statistical analysis

Data collected was managed on a Microsoft Office Excel spreadsheet. Discrete variables were expressed in percent and continuous variables were expressed as mean ± standard deviation. Chi-square test was used to assess the significance of any difference between the two groups in discrete variables.

  Results Top

A total of 500 VFs were analyzed out of which normal fields were 60. The unreliable VFs were 40 which were excluded from the study as per exclusion criteria. Age of the patients ranged from 9 to 92y with mean age of 60.435 ± 14.797. The study comprised 128 males and 72 females. Out of various causes of VFDs (n = 200), glaucoma caused VFDs in 119 (59.5%))

In glaucoma, the most common cause leading to VFD was paracentral scotoma (44.44%) followed by arcuate scotoma (23.42%) and Seidel scotoma (10.51%) [Table 1].
Table 1: Distribution of types of visual field defect in glaucoma

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Neurological lesions

Neurological lesions lead to VFD in 33 patients; percentage distribution as shown in [Table 2].
Table 2: Visual field defect in neurological lesions

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Visual field defects in age related macular degeneration

The VFD included central scotomas involving central 15°. Mean sensitivity of central fixation area in nine patients ranged from 8.652 to 14.567 ± 2.356. Mean sensitivity of peripheral area ranged from 15.657 to 21.786 ± 5.789.

In our study, VFD due to age-related macular degeneration (ARMD) were present in age group of 60–69 (n = 6) whereas 3 patients aged >70 years had ARMD VFDs. None of the patients <50 years had VFD due to ARMD.

Visual field defects in anterior ischemic optic neuropathy

VFD in anterior ischemic optic neuropathy (AION) constituted altitudinal defects occurring in 4 of our patients. All the 4 patients were in age group of 50–59 years. The difference of mean sensitivity between upper and lower hemifield in 4 patients [Table 3]. Two patients had superior altitudinal VFD, 2 patients had inferior altitudinal defect.
Table 3: Mean sensitivity difference between upper and lower hemifield

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Visual field defects due to retinitis pigmentosa

RP leads to VFD in 3 of patients with all three patients having peripheral constriction of VF and leaving central tubular vision intact.

Visual field defects due to optic neuritis

Optic neuritis leads to VFD in 3 patients (2 male and 1 female). The types of VFD were central scotoma, centrocecal scotoma, and absolute VFD [Table 4].
Table 4: Distribution of mean sensitivity in central (0°-15°) and peripheral (15°-30°) portion of visual field defect

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Thereby showing that in 2 patients mean sensitivity in central field is less than the peripheral field. The third patient having absolute VFD.

Diabetic retinopathy and branch retinal vein occlusion leading to visual field defects

Diabetic retinopathy (DR) leads to VFD in 6 patients. The patients had mild nonproliferative DR (NPDR) (n = 1), moderate NPDR (n = 3), and severe NPDR (n = 2). Distribution of VFD in DR showed diffuse depression of mean sensitivity (n = 1), paracentral scotoma (n = 3), and arcuate scotoma (n = 2).

Branch retinal vein occlusion (BRVO) caused VFD in 8 patients (6 males and 2 females). The occlusion involving inferotemporal branch of central retinal vein (n = 2) had superior arcuate scotoma and those involving superotemporal branch of central retinal vein occlusion (CRVO) (n = 2) had inferior arcuate scotoma. Other patients had paracentral scotomas corresponding to areas having vein occlusion.

Visual field defects due to cataract

Fifteen patients had VFD only due to cataract (8 males and 7 females). The VFD included diffuse depression of mean sensitivity (n = 10), central scotoma (n = 8) due to central nuclear cataract, paracentral scotomas (n = 7).

  Discussion Top

VF testing is performed for several different purposes such as to detect the presence of suspected abnormality (glaucomatous defects or hemianopias), to diagnose the cause of a visual loss and to quantitate the degree of visual loss as a baseline to detect future progression.

For these several tasks there may be different strategies. With automated perimeters, users may select the appropriate stimulus duration and interval according to what seems best in the patients. A fair degree of controversy has existed over the years regarding the use of screening versus threshold field strategies for detection of glaucoma.

In the present study, tendency oriented perimetry (TOP) strategy was used. Octopus static perimetry using a TOP strategy is a fast, patient-friendly and very reliable screening tool for the general ophthalmological practice.[4] We conducted retroprospective analysis of VF to study the causes of VF loss and types of VFD.

In our study in glaucoma, the most common cause leading to VFD was paracentral scotoma (44.44%) followed by arcuate scotoma (23.42%) and Seidel scotoma (10.51%) The superior and inferior poles of the optic nerve head are most vulnerable to glaucomatous damage. It has been postulated that these areas may be watershed areas at the junction of the vascular supply from adjacent ciliary vessels. Ultrastructural examination of the lamina cribrosa shows that the pores in the superotemporal and inferotemporal areas are larger. These larger pores may make these regions more vulnerable to compression.

Damage to the inferior and superior poles of the nerve results in loss of the arcuate nerve fiber bundles. The resulting VFD types include paracentral, arcuate, and nasal step. The inferior pole of the optic nerve appears to be more vulnerable to damage than the superior poles, so that defects occur more commonly in the superior half of the VF.

VFDs measured using standard clinical perimetry are a direct expression of the neural losses caused by glaucoma, in which the quantitative relationship varies with retinal eccentricity. The eccentricity dependence of structure-function relationships is a consequence of the normal variation in ganglion cell density with retinal eccentricity, whereas at any given distance from fixation, the standard perimetric measures of visual sensitivity (decibel units) provide an accurate estimation of ganglion cell density in comparable decibel units.[5]

The knowledge of the relationship between structural and functional damage in glaucoma may be helpful in understanding the pathogenesis of the disease and in observing the progress of the disease over a period. This relationship has been measured with sensory tests and various imaging techniques. Significant correlations have been described between perimetric tests and optic disc parameters, such as the area of the neuroretinal rim or the nerve fiber layer thickness.[6]

Differential diagnosis of glaucomatous VFDs incudes tilted disc, optic neuritis, and chiasmal lesions. In tilted discs, we have superior arcuate defects similar to those produced in glaucoma. However, they are peripheral, and not related to the blind spot. If on the other hand glaucoma developed in an eye with a tilted disc, the resulting defects relate to the blind spot, and are central. Careful inspection of the optic disc will allow for correct interpretation of the field results. In central scotoma due to optic neuritis, there is papillomacular bundle defect that crosses the horizontal line. It is associated with reduced visual acuity, and reduced color vision. It regresses with treatment, but remains central.

In bitemporal hemianopic defect due to chiasmal lesions, these can easily be confused with glaucoma, especially if the two pathologies coexist in the same patient (glaucoma plus pituitary tumor).[7]

In neurological lesions in our study, the most common neurological VFD was right lower quadrantanopia (n = 9) followed by bitemporal hemianopia resulting from the damage at the crossing of nasal fibers of optic chiasma due to pressure atrophy.

A spectrum of visual manifestations has been reported with these tumors, ranging from the absence of any visual symptoms to severe VFDs and loss of vision. The prevalence of VFDs in pituitary adenomas varies from 37% to 96% in different studies. The most common VFD is bitemporal hemianopia. However, other types of VFDs may also be observed.[8] Farooq et al.[9] found pituitary adenomas as the most common tumors of pituitary. Suchoff et al.[10] in their study to know the frequency of occurrence, types and character of VFD in acquired brain injury found traumatic and CVA to be the major causes. The VFD are scattered, restricted, homonymous, and nonhomonymous VFD. In traumatic brain injury, the most common VFD is scattered followed by homonymous defect. In CVA the most common is homonymous VFD followed by scattered and nonhomonymous VFD.[10]

Visual field defects in age-related macular degeneration

In our study, 9 patients of ARMD had VFD. In age group 60–69 years, VFD was seen in 6 patients and in >70 years, 3 patients had VFD due to ARMD. The VFD was central and paracentral scotomas and was found within 15° of central fixation point. Mean sensitivity of central 15° in 9 patients ranged from 8.652 to 14.567 ± 2.356. Mean sensitivity of peripheral area (15°–30°) ranged from 15.657 to 21.786 ± 5.789.

Nazemi et al.[11] used recently devised three dimensional computer-based threshold Amsler grid test to identify typical patterns of VFD caused by AMD. They were classified by its slope, location, shape and depth. The three dimensional depiction consistently demonstrated central scotomas with scallop-shaped and step like patterns with either steep slopes or combination of steep and shallow slopes. The steep slopes correspond to nonexudative AMD while shallow slopes indicate exudative AMD.

Visual field defects in optic neuritis and anterior ischemic optic neuropathy

Optic neuritis leads to VFD in 3 patients; (2 males and 1 female). The types of VFD were central scotoma (n = 1), centrocecal scotoma (n = 1), and absolute VFD (n = 1). Focal demyelination, inflammation, scar formation, and axonal destruction of optic nerve leads to central and centrocecal scotoma in optic neuritis.

Nevalainen et al.[12] studied VF from 99 individuals with clinically diagnosed optic neuritis were evaluated. Central scotoma was the most common finding in associated eyes covering 41% of all VFD in affected eyes. Nerve fiber bundle defects were found in 29% and paracentral scotoma in 14% of all VFD.

According to the study by Keltner et al.[13] diffuse and central loss were more predominant in the affected eye at baseline, and nerve fiber bundle defects (partial arcuate, paracentral, and arcuate) were the most predominant localized abnormalities in both the affected and fellow eyes.

The VFD in AION constituted altitudinal defects occurred in 4 of our participants. Hemianopia usually occurs in the lower VF and less commonly in the upper half. The demarcation line lies horizontally and may not be absolutely straight. The pathogenesis of these defects has evoked many ingenious hypotheses.

They are due to acute circulatory disorders of the optic nerve in posthemorrhagic amaurosis and ischemic optic neuropathy.

It has been suggested that injury to the blood supply of the optic nerve produced altitudinal hemianopia, usually inferior. It is proposed that a sharp division of the optic nerve into three areas based on its blood supply-superior peripheral, inferior peripheral, and central. It is stated that the vascular supply to the optic nerve came through a network of vessels in the arachnoid membrane, which passed through the subarachnoid space and entered the optic nerve at right angles. In its upper part the space is narrow and the vessels that traverse it from the membrane to the nerve are short and easily damaged by torsion, edema, and other injury. This, according to Harrington (1964), gives rise to a unilateral altitudinal field defect with horizontal border, steep edges, and great density.

Hayreh (1970) stated that occlusion of one of the two main posterior ciliary arteries, which supplies half of the optic disc and the corresponding choroid, produces an altitudinal field defect with no retinal changes at all. In acute occlusive disorders, the corresponding half of the disc will be edematous at first, with evidence of ischemic neuropathy in that part of the disc. Later, all cases show optic atrophy of the corresponding half of the disc.

Retinitis pigmentosa

In our study, VFD was seen in 3 of our individuals with all individuals having peripheral constriction of VF and sparing of Central Island. The individuals initial pattern of VF loss could not be categorized due to advanced stage of VFL at the time of initial examination.

Kinetic VFs begin to constrict after a critical age, but the annual rate of decline varies from 5% to 20% depending on the isopter and RP genotype. Static perimetry, which evolved primarily for the detection of glaucomatous field defects, has also been used as a primary outcome measure in clinical trials in RP.[14]

According to Sugawara et al.[15] the VFL was graded from Grade 0 to Grade 6. Grade 0 of normal VF to Grade 6 constriction of VF within central 10°. Our patients fall in Grade 6 with constriction of VF within central 10°.

Visual field defects due to cataract

VFD due to cataract was diffuse and present in 15 individuals (8 males and 7 females). Eight individuals had central VFD, 7 individuals had paracentral VFD. Cataracts are known to depress the overall sensitivity of the VF, but localized VFDs due to cataract are extremely rare.

Media opacities are known to cause VFDs, the degree of which varies from generalized depression of the VF to apparent scotomatous areas. These opacities necessitate a posterior position in the lens to produce a relative scotoma. An opacity in the media anteriorly placed produce generalized reduction in the VF.

Cataracts are thought to cause visual degradation by 3 mechanisms: image blur, light scattering, and decreased illumination. Investigation of the effect of cataract or light scattering (simulated cataract) on the VF has generally shown that cataract results in diffuse reduction of sensitivity in healthy controls. Although the pattern of sensitivity loss may not be entirely uniform across the VF, predominantly localized field loss such as that frequently seen in glaucoma is unlikely to be related to cataract.[16]

It has been stated that cataract does not produce dense scotoma on automated perimetry. However, it does produce relative scotomas actual glaucomatous VFD may be hidden to some extent.

Visual field defects due to diabetic retinopathy

DR leads to VFD in 6 patients (2 male, 4 female). Diffuse depression of mean sensitivity occurred in 3 patients aged 50–59 ranging from 19.025 ± 4.521, paracentral scotomas in 2 patients and altitudinal defect in 1 patient. These findings showed that in diabetic patients VFDs correlated with the extent of retinal vascular compromise. This can be detected in patients with moderate retinopathy, and occur more frequently in noninsulin-dependent patients than in insulin-dependent patients, and may result from subclinical microangiopathy.

The most widely used test of retinal dysfunction is standard automated perimetry (SAP), which has rendered results indicating a reduction of retinal sensitivity in diabetic individuals without retinopathy as well as in those with mild/moderate or moderate/severe retinopathy. Moreover, reduction of retinal sensitivity revealed by SAP was found to correlate with stepwise increases in the severity of retinopathy.[17] In the posterior segment, there is evidence that RNFL thinning, VF deficits and abnormal visual electrophysiology results can occur in the absence of clinically evident retinopathy.[18] This suggests that neuropathic changes observed in the eye might be occurring as a direct result of the metabolic compromises of diabetes and not necessarily as a secondary complication of vasculopathy. Certainly, van Dijk et al.[19] came to a similar conclusion based on their observations of decreased retinal ganglion cell layer thickness in patients with type 1 diabetes and minimal retinopathy.

Visual field changes due to branch retinal vein occlusion

VFD due to BRVO occurred in 8 patients (6 males and 2 female). The field defects include superior arcuate scotoma (n = 2), inferior arcuate scotoma (n = 2), superotemporal paracentral scotoma (n = 1), and inferotemporal paracentral scotoma (n = 1). BRVO affecting the upper/outer portion (superotemporal quadrant) of the retina thus lead to the sensation of blurring or missing vision just below the central visual axis (retinal and VFs are inversely related) whereas BRVO involving inferotemporal quadrant lead to VFD superiorly.

VFDs such as central scotomas, paracentral scotomas, nerve fiber bundle scotomas, and segmental peripheral constriction patterns have been reported in the patients of BRVO.[20]

The present retroprospective study concludes that, most of the patients for whom perimetry was performed on Octopus 900 perimeter under ocular conditions, the glaucoma was the most common disease. The second most common cause of VFD was neurological, the common lesions being head trauma, CVA, and pituitary adenomas. The other ocular causes of VFD were cataract, ARMD, BRVO, CRVO, DR, AION, RP, and optic neuritis. Therefore, the stimulus for this work was not only ophthalmological but also neurological although more number of individuals and long-term analysis of VF will be required in confirming the disease and VF pattern distribution of ocular and systemic diseases.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Morales J, Weitzman ML, González de la Rosa M. Comparison between tendency-oriented perimetry (TOP) and octopus threshold perimetry. Ophthalmology 2000;107:134-42.  Back to cited text no. 1
Mills RP, Budenz DL, Lee PP, Noecker RJ, Walt JG, Siegartel LR, et al. Categorizing the stage of glaucoma from pre-diagnosis to end-stage disease. Am J Ophthalmol 2006;141:24-30.  Back to cited text no. 2
Thomas R, Shenoy K, Seshadri MS, Muliyil J, Rao A, Paul P, et al. Visual field defects in non-functioning pituitary adenomas. Indian J Ophthalmol 2002;50:127-30.  Back to cited text no. 3
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Scherrer M, Fleischhauer JC, Helbig H, Johann Auf der Heide K, Sutter FK. Comparison of tendency-oriented perimetry and dynamic strategy in octopus perimetry as a screening tool in a clinical setting: A prospective study. Klin Monbl Augenheilkd 2007;224:252-4.  Back to cited text no. 4
Harwerth RS, Quigley HA. Visual field defects and retinal ganglion cell losses in patients with glaucoma. Arch Ophthalmol 2006;124:853-9.  Back to cited text no. 5
Horn FK, Mardin CY, Laemmer R, Baleanu D, Juenemann AM, Kruse FE, et al. Correlation between local glaucomatous visual field defects and loss of nerve fiber layer thickness measured with polarimetry and spectral domain OCT. Invest Ophthalmol Vis Sci 2009;50:1971-7.  Back to cited text no. 6
Yaqub M. Visual fields interpretation in glaucoma: A focus on static automated perimetry. Community Eye Health 2012;25:1-8.  Back to cited text no. 7
Dhasmana R, Nagpal RC, Sharma R, Bansal KK, Bahadur H. Visual fields at presentation and after trans-sphenoidal resection of pituitary adenomas. J Ophthalmic Vis Res 2011;6:187-91.  Back to cited text no. 8
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Suchoff IB, Kapoor N, Ciuffreda KJ, Rutner D, Han E, Craig S, et al. The frequency of occurrence, types, and characteristics of visual field defects in acquired brain injury: A retrospective analysis. Optometry 2008;79:259-65.  Back to cited text no. 10
Nazemi PP, Fink W, Lim JI, Sadun AA. Scotomas of age-related macular degeneration detected and characterized by means of a novel three-dimensional computer-automated visual field test. Retina 2005;25:446-53.  Back to cited text no. 11
Nevalainen J, Krapp E, Paetzold J, Mildenberger I, Besch D, Vonthein R, et al. Visual field defects in acute optic neuritis – Distribution of different types of defect pattern, assessed with threshold-related supraliminal perimetry, ensuring high spatial resolution. Graefes Arch Clin Exp Ophthalmol 2008;246:599-607.  Back to cited text no. 12
Keltner JL, Johnson CA, Cello KE, Dontchev M, Gal RL, Beck RW, et al. Visual field profile of optic neuritis: A final follow-up report from the optic neuritis treatment trial from baseline through 15 years. Arch Ophthalmol 2010;128:330-7.  Back to cited text no. 13
Birch DG, Locke KG, Wen Y, Locke KI, Hoffman DR, Hood DC, et al. Spectral-domain optical coherence tomography measures of outer segment layer progression in patients with X-linked retinitis pigmentosa. JAMA Ophthalmol 2013;131:1143-50.  Back to cited text no. 14
Sugawara T, Hagiwara A, Hiramatsu A, Ogata K, Mitamura Y, Yamamoto S. Relationship between peripheral visual field loss and vision-related quality of life in patients with retinitis pigmentosa. Eye (Lond) 2010;24:535-9.  Back to cited text no. 15
Carrillo MM, Artes PH, Nicolela MT, LeBlanc RP, Chauhan BC. Effect of cataract extraction on the visual fields of patients with glaucoma. Arch Ophthalmol 2005;123:929-32.  Back to cited text no. 16
Hellgren KJ, Agardh E, Bengtsson B. Progression of early retinal dysfunction in diabetes over time: Results of a long-term prospective clinical study. Diabetes 2014;63:3104-11.  Back to cited text no. 17
Efron N. The Glenn A. Fry award lecture 2010: Ophthalmic markers of diabetic neuropathy. Optom VisSci2011;88:661-83.  Back to cited text no. 18
van Dijk HW, Verbraak FD, Kok PH, Garvin MK, Sonka M, Lee K, et al. Decreased retinal ganglion cell layer thickness in patients with type 1 diabetes. Invest Ophthalmol Vis Sci 2010;51:3660-5.  Back to cited text no. 19
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  [Table 1], [Table 2], [Table 3], [Table 4]


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