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ORIGINAL ARTICLE
Year : 1995  |  Volume : 43  |  Issue : 3  |  Page : 127-130

Relative afferent pupillary defect and edge light pupil cycle time in the early differentiation of central retinal vein occlusion


From Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi 110 029, India

Correspondence Address:
Vimala Menon
From Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi 110 029
India
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Source of Support: None, Conflict of Interest: None


PMID: 8822487

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  Abstract 

A total of 37 patients of unilateral fresh central retinal vein occlusion (CRVO) of less than one month duration were examined and re-evaluated after 8 weeks. All eyes with relative afferent pupillary defect (RAPD) ≤0.6 log units with edge light pupil cycle time (ELPCT) of 925 94 ms, visual acuity ≥ 6/60 with minimal field defects proved to be of nonischemic CRVO, while eyes with RAPD ≥ 0.9 log units with ELPCT of 4005 712 ms, visual acuity 3/60 with marked field defects proved to be of ischemic CRVO with evidence of retinal ischemia on fluorescein angiography. RAPD and ELPCT were found to be extremely reliable indicators for early differentiation of ischemic from nonischemic CRVO and the values remained stable over a period of time. The electroretinography (ERG) correlated well with these parameters.

Keywords: Relative afferent pupillary defect - Edge light pupil cycle time -Central retinal vein occlusion.


How to cite this article:
Menon V, Nachiketa, Kumar A. Relative afferent pupillary defect and edge light pupil cycle time in the early differentiation of central retinal vein occlusion. Indian J Ophthalmol 1995;43:127-30

How to cite this URL:
Menon V, Nachiketa, Kumar A. Relative afferent pupillary defect and edge light pupil cycle time in the early differentiation of central retinal vein occlusion. Indian J Ophthalmol [serial online] 1995 [cited 2020 Jun 5];43:127-30. Available from: http://www.ijo.in/text.asp?1995/43/3/127/25285



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Despite central retinal vein occlusion (CRVO) being a common clinical entity, controversies persist regarding its diagnosis, differentiation, prognosis and management.

CRVO is of two distinct entities, the nonischemic CRVO which usually runs a benign course and the ischemic CRVO which has a poorer prognosis with more than half of these eyes ultimately developing neovascular glaucoma.[1],[2]

Hayreh et al[3],[4] in their classic studies of CRVO found measurement of relative afferent pupillary defect (RAPD) as a very sensitive and specific indicator in the early differentiation of ischemic CRVO.

The edge light pupil cycle time (ELPCT) described by Miller and Thompson[5],[6] is a useful test for measuring the afferent and efferent pupillary defects. Though the ELPCT is known to be affected in optic nerve affections, it has never been studied in CRVO. Hence, we attempted to measure the ELPCT along with RAPD and other parameters in patients with fresh CRVO.


  Materials and methods Top


A prospective clinical study of 37 patients suffering from fresh CRVO in one eye of less than one month duration was undertaken and these patients were followed up for re-evaluation after a period of eight weeks. Eyes with macular and optic nerve diseases, proliferative retinopathies or other disorders affecting vision were excluded from the study.

After obtaining a detailed ocular and systemic history, the patients underwent a thorough ocular examination including best-corrected visual acuity, slit-lamp anterior segment biomicroscopy, applanation tonometry, gonioscopy, direct and indirect ophthalmoscopy. The RAPD was measured by the "swinging flash light" test utilising neutral density filters of graded log unit densities.[7] The ELPCT was measured as described by Miller and Thompson.[5] A horizontal slit-lamp beam of 0.5 x 5 mm was focussed from below to the pupillary edge causing alternating cycles of constriction and dilation of the pupil. The time taken by 100 cycles (two runs of 50 cycles each) in seconds was multiplied by ten to obtain the ELPCT in milliseconds.

The patients also underwent fluorescein angiography, visual field charting and electroretinography (ERG). These tests were repeated at the 8-week follow-up visit.

Statistical analysis was done using Student's t-test, paired t-test, multiple range test, analysis of one-way variance (ANOVA) and hypothesis test.


  Results Top


A total number of 37 eyes with fresh CRVO of less than one month duration, with the fellow normal eye serving as control, were examined and re-evaluated at the 8-week follow-up visit.

A total of 16 eyes (43.5%) had RAPD of ≤ 0.6 log units and 21 eyes (56.5%) had RAPD of ≥ 0.9 log units [Figure - 1].

Eyes with RAPD ≤0.6 log units had a mean ELPCT of 925 94 ms at the initial visit, while eyes with RAPD ≥ 0.9 log units had a mean ELPCT of 4005 712 ms. The ELPCT on follow-up visit was 928 105 for eyes with RAPD ≤0.6 log units and 4311 799 for eyes with RAPD ≥0.9 log units. Thus, no significant difference between the initial and follow-up ELPCT was seen in the two groups [Figure - 2]. The difference in the mean ELPCT between the eyes with RAPD ≤ 0.6 log units and RAPD ≥ 0.9 log units was found to be statistically significant (p = < 0.001).

All eyes with RAPD ≤ 0.6 log units had a mean visual acuity of 6/60 or better which improved to 6/18 or better at the follow-up visit, while all eyes with RAPD ≥ 0.9 log units had an initial visual acuity of ≤ 3/60 which worsened subsequently (Table).

Fluorescein angiography at the initial visit did not reveal any significant findings in most of the eyes due to extensive surface retinal haemorrhages. However, on follow-up after eight weeks, three of the eyes with RAPD ≤ 0.6 log unit occasionally showed isolated capillary nonperfusion areas, while most of the eyes with RAPD ≥ 0.9 log units showed large areas of capillary nonperfusion, with more than half of these cases having areas of capillary nonperfusion greater than 10 disc diameters.

On ophthalmoscopic examination, it was difficult to distinguish between ischemic and nonischemic CRVO, both at the initial and follow-up visits.

Visual field examination showed mild enlargement of blind spot with slight constriction of fields and occasional relative scotomas in eyes with RAPD ≤ 0.6 log units while eyes with RAPD ≥ 0.9 log units showed marked field constriction with dense central scotoma in almost all cases both at the initial and eight-week follow-up visits.

Electroretinography revealed that the patients with RAPD ≤ 0.6 log units had a mean b/a amplitude ratio values of 1.9 0.33, while eyes with RAPD ≥ 0.9 log units had a mean b/a value of 1.37 0.25. This difference between both the groups was found to be significant (p = < 0.001).


  Discussion Top


CRVO is a common clinical entity, first described over 150 years ago. Our understanding of CRVO has evolved considerably during the past quarter of a century, mainly because of better diagnostic procedures including fluorescein fundus angiography, ERG and other refined tests, such as, perimetry and measurement of RAPD.

The evidence from clinical[1],[2],[8][9][10] and experimental[11][12][13]studies show unequivocally that CRVO is of two distinct entities - one without retinal ischemia (nonischemic type) and the other accompanied by retinal ischemia (ischemic type). The two types of CRVO have different natural histories,[2],[14][15][16][17] prognosis and management.[18][19][20][21]But differentiation between nonischemic and ischemic types of CRVO remains controversial. Most investigators have so far mainly used ophthalmoscopy and fluorescein fundus angiography in the differentiation of CRVO. Typical signs of ischemic CRVO consists of extensive superficial retinal haemorrhages and cotton-wool spots on ophthalmoscopy and retinal capillary nonperfusion or obliteration on fluorescein angiography.[1][2][3],[9]

The retinopathy produced by CRVO (both ischemic and non-ischemic) is a constantly evolving process and hence, the ophthalmoscopic and fluorescein fundus angiographic findings change with the age of the retinopathy.

The primary interest in distinguishing the type of CRVO during its early acute stages is to identify ischemic CRVO which is known to cause anterior segment neovascularization.

Hayreh et al[1][2][3][4] in their prospective, long-term, longitudinal natural history studies have shown how both ophthalmoscopy and fluorescein fundus angiography have a scientifically unacceptable margin of error in differentiating ischemic from nonischemic CRVO during the early stages of the disease. However, they found measurements of RAPD and ERG to be the most reliable and sensitive indicator for the early differentiation of CRVO into ischemic and nonischemic types.

Depending on the type of CRVO and associated complications, the visual acuity may range from 6/6 to light perception. The vision may be decreased due to macular oedema, detachment or haemorrhage, capillary nonperfusion, vitreous haemorrhage, or rarely, arteriolar occlusion.

Earlier studies have shown that the nonischemic CRVO has better initial and final visual acuities compared to ischemic CRVO. Magargal et al[9] found that 82% of patients with good capillary perfusion had an initial visual acuity of 6/60 or better, and 34% had 6/12 or better vision. According to Fong et al,[16] 47% of patients with nonischemic CRVO had 6/12 or better vision and only 28% were worse than 6/60, while in patients with ischemic CRVO, 45% had visual acuity of 3/60 or worse. Initial visual acuity thus appears to be reasonably correlated with the type of CRVO based on the degree of capillary perfusion.

In our study, the eyes with nonischemic CRVO had initial acuities of 6/60 or better with 69% of these having a visual acuity of 6/12 or better, while all the eyes of ischemic CRVO with RAPD of ≥ 0.9 log units had initial visual acuity of 3/60 or less.

Measurement of RAPD has proven value in the prediction of visual field loss in certain optic nerve and retinal diseases.[22] Since 94% of patients with CRVO have only one eye involved and the visual field loss is markedly different between the two types of CRVO, RAPD has been found to be a very sensitive and specific test as a predictor of ischemia and in differentiation of CRVO. Hayreh et al[1] and Servais[3] have found the sensitivity and specificity for detection of ischemic CRVO to be 88% and 90%, respectively, when RAPD of ≥ 0.7 log units of neutral density filters was used as a cut off.

In our study of 37 eyes, all eyes with RAPD ≤ 0.6 log units proved to be cases of nonischemic CRVO, while all eyes with RAPD ≥ 0.9 log units had ischemic CRVO with definite signs of ischemia on fluorescein angiography at the 8-week follow-up visit.

The ELPCT in normal eyes was 822 69 ms. Prolonged ELPCT has been found in cases of optic neuritis and other optic nerve pathologies.[6] In this study, all eyes of nonischemic CRVO with RAPD ≤ 0.6 log units had a mean ELPCT of 925 94 ms at the initial visit compared with eyes of ischemic CRVO that had a mean ELPCT of 4005 712 ms. There was no significant change in the initial and follow-up ELPCT. In the eyes with RAPD ≥ 1.2 log units, it was difficult to count the cycles.

The ELPCT was probably affected due to inner retinal ischemia and damage to the nerve fibre layer, causing a conduction defect. Thus, the extent of ischemia is reflected in the severity of conduction defect in the form of markedly raised ELPCT and RAPD values. The ELPCT when affected in optic neuritis returns to normal (Cox et al, 1982) but in CRVO it continues to be abnormally increased.

The presence of retinal capillary obliteration on fluorescein angiography is the principle difference in the differentiation of ischemic from nonischemic CRVO, which takes 3 to 4 weeks to develop.[1][2][3][4]

We found that apart from eyes with no RAPD and few with RAPD of 0.3 log units, it was very difficult and nearly impossible to differentiate between the two types of CRVO by fluorescein angiography at the early stage. All eyes with RAPD ≥ 0.9 log units showed extensive areas of capillary non-perfusion on the eight-week follow-up fluorescein angiography as compared with eyes of nonischemic CRVO with RAPD ≤0.6 log units which occasionally showed isolated areas of capillary nonperfusion. Thus, fluorescein angiography could only differentiate between the two types of CRVO with reasonable accuracy only at the 8-week follow-up visit.

The retinal haemorrhages which constitute an invariable finding in CRVO vary markedly not only from eye to eye (in both ischemic and nonischemic CRVO) but also with time since onset. We found ophthalmoscopy to be the least reliable method of differentiating ischemic from nonischemic CRVO at an early stage. All eyes of ischemic CRVO showed marked constriction of visual fields with dense central scotomas, while eyes of nonischemic CRVO showed minimal field defects both at the initial and 8-week follow-up visits. This was similar to earlier studies.[1][2][3][4],[16]

Electroretinography in CRVO was first used by Karpe in 1946[23] and since then has been shown to be a reliable objective test in the differentiation of ischemic from nonischemic CRVO. Several investigators[24][25][26][27] have shown that the b/a amplitude ratio is markedly reduced in ischemic CRVO compared with non-ischemic CRVO. In this study, the eyes having ischemic CRVO had a mean value of 1.37 0.25 as compared to non-ischemic cases with a mean value of 1.9 0.33, which was found to be significant (p = < 0.001).

After measuring the RAPD and ELPCT in 37 patients of fresh CRVO and comparing them with other parameters, we conclude that measurement of RAPD is a simple, inexpensive, objective, sensitive and specific test in the early differentiation of CRVO. The ELPCT was found to be a better objective indicator of ischemic CRVO. Both these tests fared better when compared to other morphological tests, such as, fluorescein angiography and ophthalmoscopy, in the early differentiation between ischemic and nonischemic CRVO.

The visual acuity, visual fields and ERG correlated well with the affections of RAPD and ELPCT.

 
  References Top

1.
Hayreh SS, Klugman MR, Beri M, et al. Differentiation of ischemic from non-ischemic CRVO during the early acute phase. Graefe's Arch Ophthalmol 228:201-217,1990.  Back to cited text no. 1
    
2.
Hayreh SS, Rohas P, Podhajsky P, et al. Ocular neovascularization with retinal vascular occlusion III. Ophthalmology 90:488-506,1983.  Back to cited text no. 2
    
3.
Servais GE, Thompson HS, Hayreh SS. Relative afferent pupillary defect in central retinal vein occlusion. Ophthalmology 100:24-30,1993.  Back to cited text no. 3
    
4.
Hayreh SS, Klugman MR, Podhajsky P, Kolder HE. ERG in CRVO:Correlation of ERG changes with pupillary abnormalities. Graefe's Arch Clin Ophthalmol 227:549-591,1989.  Back to cited text no. 4
    
5.
Miller SD, Thompson HS. Edge light pupil cycle time. Br J Ophthalmol 62:495-500, 1978.  Back to cited text no. 5
    
6.
Miller SD, Thompson HS. Pupil cycle time in optic neuritis. Am J Ophthalmol 85:635,1978.  Back to cited text no. 6
    
7.
Thompson HS, Corbett JJ, Cox TA. How to measure relative afferent pupillary defect. Surv Ophthalmol 26:39-42, 1981.  Back to cited text no. 7
    
8.
Hayreh SS. So-called CRVO II. Venous stasis retinopathy. Ophthalmologica 172:14-37,1976.  Back to cited text no. 8
    
9.
Magargal LE, Brown GC, Augsburger JJ, Parrish RK:II NVG following CRVO. Ophthalmology 88:1095-1101, 1981.  Back to cited text no. 9
    
10.
Zegarra H, Gutman FA, Conforto J. The natural course of CRVO. Ophthalmology 86:1931-1942, 1979.  Back to cited text no. 10
    
11.
Hayreh SS. An experimental study of CRVO. Trans Ophthalmol Soc UK 84:586-595,1964.  Back to cited text no. 11
    
12.
Hayreh SS. Pathogenesis of occlusion of the central retinal vessels. Am J Ophthalmol 72:998-1011,1971.  Back to cited text no. 12
    
13.
Green WR, Chan CC, Hutchins GM, Terry JM. Central retinal vein occlusion:A prospective histopathologic study. Retina 1:27-55,1981.  Back to cited text no. 13
    
14.
Walters RF, Spalton DJ. Central retinal vein occlusion in people aged 40 years or less. A review of 17 patients. Br J Ophthalmol 74:30-35,1990.  Back to cited text no. 14
    
15.
Clarkson JG. Central vein occlusion study (CVOS). National Eye Institute Publications, 1988.  Back to cited text no. 15
    
16.
Andrew CO Fong, Schatz H. CRVO in young adults. Surv Ophthalmol 37:393-417,1993.  Back to cited text no. 16
    
17.
Baseline and early natural history report:The central vein occlusion study. Central Vein Occlusion Study Group. Arch Ophthalmol 111:1087-1095, 1993.  Back to cited text no. 17
    
18.
Magargal LE, Brown GC, Augsburger JJ, Donoso LA. Efficacy of PRP in preventing NVG following ischemic CRVO. Ophthalmology 89:780-784,1982.  Back to cited text no. 18
    
19.
Kohner EM, Laatikainen L, Oughton J. The management CRVO. Ophthalmology 90:484-487,1983.  Back to cited text no. 19
    
20.
Klein ML, Finkelstein D. Macular grid photocoagulation for macular oedema in CRVO. Arch Ophthalmol 107:1297-1302, 1989.  Back to cited text no. 20
    
21.
Welch JC, Augsberger JJ. Assessment of angiographic retinal capillary nonperfusion in CRVO. Am J Ophthalmol 103:761-766, 1987.  Back to cited text no. 21
    
22.
Cox TA, Thompson HS. RAPD in optic neuritis. Am J Ophthalmol 105:141-146,1981.  Back to cited text no. 22
    
23.
Karpe G, et al. The prognostic value of ERG in thrombosis of the retinal veins. Acta Ophthalmol (suppl) 70:202-229, 1962.  Back to cited text no. 23
    
24.
Sabates R, Hirose T, McMeel JW. Electroretinography in the prognosis and classification of central retinal vein occlusion. Arch Ophthalmol 101:232-235, 1983.  Back to cited text no. 24
    
25.
Barber C, et al. The role of ERG in management of CRVO. Doc Ophthalmol Proc Ser 40:149-159,1989.  Back to cited text no. 25
    
26.
Kaye SB, Harding SP. Early electroretinography in unilateral central retinal vein occlusion as a predictor of rubeosis iridis. Arch Ophthalmol 106:353-356, 1988.  Back to cited text no. 26
    
27.
Johnson MA, Marcus S, Elman MJ, McPhee TJ. Neovascularization in central retinal vein occlusion in young adults:Electroretinographic findings. Arch Ophthalmol 106:348-352,1988.  Back to cited text no. 27
    


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