Abstract
purpose. Strabismus may be associated with an asymmetry of monocular horizontal optokinetic nystagmus (OKN). It is unclear whether OKN asymmetries are associated with deficiency in binocular and/or stereovision. In the current study, patients with different degrees of binocularity were investigated.
methods. OKN was examined in the dominant and nondominant eyes of four groups of patients: (1) no measurable binocularity (NB), (2) poor binocularity (PB)—that is, showing binocularity on the Bagolini Test and/or rudimentary stereovision, (3) good binocularity (GB) with good stereoacuity after squint surgery, and (4) a control group. Monocular OKN was elicited with black-and-white stripes moving temporally to nasally (TN) or nasally to temporally (NT) at velocities of 15, 30, 45, and 60 deg/s. Eye movements were recorded with infrared oculography.
results. Only subjects in the NB group showed a significant OKN asymmetry, with preference for TN stimulation in dominant and nondominant eyes. Subjects with PB did not have significant OKN asymmetries but reduced OKN gains in both stimulus directions. Subjects with GB had normal mean OKN gains without asymmetry. Larger OKN asymmetries were correlated with younger age at detection of strabismus if NB and GB were grouped together, but not if each group was analyzed separately.
conclusions. For the first time, a large groups of patients classified by level of binocular vision has been investigated. The results show that OKN gain and asymmetry are associated with the development of binocular vision. OKN investigation may be helpful to identify patients with binocularity or binocular potential in strabismus.
OKN is a rhythmic involuntary eye movement elicited by large moving patterns.
1 It consists of a slow component with eye movements in the same direction as the movement of a target and a fast component with saccadic eye movements in the opposite direction.
2 OKN can be quantified by measuring the gain, which corresponds to the ratio of slow-phase eye velocity and stimulus velocity.
Horizontal OKN asymmetry is evident in early normal infancy,
3 4 and in patients who have normal visual development disrupted by unequal visual inputs from the two eyes due to strabismus,
5 amblyopia,
6 or unilateral congenital cataracts.
7 This asymmetry of OKN is due to a larger gain elicited by temporal to nasal (TN) stimulus motion compared with nasal to temporal (NT) stimulus motion when the stimulation is applied monocularly.
8 Hoffmann
9 hypothesized that horizontal TN OKN present early in life is mediated entirely by subcortical projections to the pretectal nucleus of the optic tract (NOT) and the dorsal terminal nucleus (DTN) of the accessory optic system. Cortical projections to NOT-DTN develop later, and, once established, the subcortical projections lose influence over NOT-DTN cells. Thus, the increasing dominance of the cortex allows the development of the symmetrical OKN response in normal subjects. OKN symmetry and binocular vision in infants develop simultaneously.
3 4 If binocular vision is disrupted, it is likely that subcortical pathways, which favor nasalward motion, will dominate.
It has been reported that the OKN deficit is more prevalent when strabismus manifests itself early, between the first 6 and 24 months of life.
5 10 11 12 13 14 15 16 However, it is usually difficult to know the exact time of onset. Most studies have examined older subjects, in whom the onset of strabismus was evaluated retrospectively, without clinical examination data available from the time of onset. Only a few studies have investigated the relationship of binocular function and OKN asymmetry, and these have suggested that there is no correlation.
12 17 18 19 One study, however, showed a relationship between stereopsis and symmetry of OKN gain.
20
In this study, our purpose was to investigate the relation between horizontal OKN asymmetries and clinical characteristics such as binocular- and stereovision, visual acuity or age of the onset of squint. OKN was examined in four groups of subjects divided according to binocular vision: (1) no measurable binocular vision (NB); (2) poor binocularity (PB) when tested on the Bagolini Test and/or gross stereopsis; (3) good binocular vision (GB) with a normal or almost normal level of postoperative stereoacuity; and (4) normal subjects. In the NB and GB groups, we selected only subjects for whom the age of onset of strabismus had been documented in our department.
The ethics committee of the Kantonsspital St. Gallen approved the study. Informed consent was obtained from all subjects after explanation of the nature of the investigation. The study was performed in accordance with the tenets of the Declaration of Helsinki.
Patients were recruited from the Department of Strabismology and Neuroophthalmology of the Kantonsspital St. Gallen. At the time of OKN examination, all subjects were old enough to cooperate easily with all tests. The subjects had no ophthalmic abnormalities other than squint or amblyopia and were otherwise healthy. A full ophthalmic examination, including visual acuity, binocular function (Bagolini test), stereoacuity (TNO test [Richmond Products, Boca Raton, FL)]and Titmus fly for gross stereopsis of 3000 seconds of arc), ocular motility, cover test, slit lamp examination, funduscopy, and cycloplegic refraction, was performed in all subjects. Patients with latent nystagmus were excluded from the study because this form of nystagmus interacts with OKN, slowing down the NT slow phase and speeding up the TN slow phase.
21
Four different groups of subjects were examined:
-
Twenty patients with no measurable binocularity (NB; 8 males, 12 females; mean age at time of OKN examination: 17.5 ± 13 years; SD). Strabismus was documented before or at 18 months of age in all patients in this group. Twelve patients had dissociated vertical deviation (DVD), and 16 had occlusion therapy for amblyopia. All subjects underwent strabismus surgery before OKN examination. After surgical correction of squint, stereopsis (measured using the Titmus fly) or binocular vision (measured by absence of suppression of the nondominant eye on the Bagolini test) was not detectable in any of the subjects of this group. Details of patients with NB are listed in
Table 1 .
-
Twenty patients with poor binocular vision (PB; 10 males, 10 females; mean age at time of OKN examination: 15.6 ± 13.9 years; SD)—that is, with peripheral fusion on Bagolini test with central scotoma and/or stereopsis measured with the Titmus fly (15 subjects). None of the patients with PB demonstrated stereopsis when examined with the TNO test. At the time of examination, they all had small squint angles, which corresponded either to primary or secondary postoperative microtropia. Ten of these patients had a history of sudden increase of squint angle when they first were examined in our department. Photographs of the patient before onset of strabismus confirmed this, although the photographs did not exclude microtropia. These patients underwent squint surgery and achieved rudimentary binocular vision after surgery. Because of the small squint angle in the PB group, strabismus was most frequently detected after the screening tests for amblyopia or because of the sudden development of a large strabismus (with possible preexistence of microtropia). Therefore, it was unlikely that the time of first examination in our department had any correlation with time of onset of squint in this group. In the PB group 10 patients had occlusion therapy for amblyopia. None of the subjects in this group had DVD. Details of patients with PB are listed in
Table 2 .
-
Fifteen patients (seven males, eight females; mean age at time of OKN examination: 10.2 ± 3.1 years; SD) who achieved binocular vision on the Bagolini test and good levels of stereovision on the TNO test (15–240 seconds of arc) at the time of examination (GB). All had late-onset strabismus and had a well-documented sudden onset of strabismus between 18 and 36 months of age. History and/or examination revealed that, shortly after onset of squint, all had diplopia or signs indicating diplopia, such as frequently closing one eye. Two patients in the GB group had eyes patched for amblyopia. None of them had DVD. All had undergone strabismus surgery and had no postoperative manifest squint. In
Table 3 further details of patients with GB are listed.
-
Twenty control subjects (8 males, 12 females; mean age 14.8 ± 7.2 years; SD) without squint or history of squint surgery, with visual acuity of 1.0 or better in each eye, and stereoacuity between 15 and 120 seconds of arc on the TNO test.
In the NB and GB groups, only patients who had been examined in our department and had well-documented clinical notes from the age of diagnoses of squint were included in the study.
In summary, we found that only subjects with NB showed significant OKN asymmetry with preference for TN stimulation rather than NT stimulation, in dominant and nondominant eyes. Asymmetries were more frequent in nondominant eyes. Subjects with PB did not have a significant preference for TN stimulation, although the OKN gain of these subjects was reduced for both stimulus directions and in both eyes. Subjects with GB had normal mean OKN gains and showed no significant preference in either stimulation direction. Larger asymmetry factors were correlated with younger age at detection of strabismus only if NB and GB were grouped together.
In the literature, OKN asymmetries have usually been analyzed in relation to onset of strabismus by comparing subjects with early-onset with those with late-onset strabismus. The age limit used to define early-onset strabismus varies in different reports from 6 months,
12 to 12 months,
13 and up to 24 months.
14 Several studies
5 10 11 12 13 14 have found a greater prevalence of asymmetry with earlier onset of strabismus. In all these studies, asymmetries were present in the dominant eyes, but were less common than in the nondominant eyes. Schor et al.
5 found that monocular OKN asymmetries could be used to predict whether esotropia had occurred before or after the first year of life. In our study, we found asymmetry in 75% to 85% of the nondominant eyes and in 50% to 65% of the dominant eyes in the NB group, depending on stimulation velocity. Strabismus onset was documented as occurring before or at 18 months of age. In the PB group, up to 30% of subjects had asymmetrical OKN with TN preference; however, some subjects also showed NT preference, reflecting a wider variation of data. Consequently, only the NB group showed significantly asymmetrical OKN as a group. Most studies have used ages estimated retrospectively for onset of strabismus. However, it is impossible to determine the exact time of onset of strabismus by these means, because onset may remain long undetected by lay people before clinical examination. Also, a slow increase in squint angle may lead to a wrong assumption of the time of onset. The difficulty in determining the exact time of onset of strabismus retrospectively may explain discrepancies between findings.
We found that OKN asymmetries were consistently but not significantly larger in patients with DVD than in subjects without DVD (probably due to the small sample size within the NB group) and appeared to increase with increasing stimulus velocities. Because DVD is a strong indicator of early-onset strabismus
5 this may also indicate a relation between earlier onset of strabismus and asymmetric OKN.
OKN responses have been reported as asymmetrical in normal children between 3 and 24 months of age
3 24 25 (Roy MS, et al.
IOVS 1987;28:ARVO Abstract 18; Lewis TL, et al.
IOVS 1991;32:ARVO Abstract 1437). Consequently, testing observers with strabismus at an older age, as in our study, may help differentiate between the normal maturation processes for OKN symmetry, and its alteration by strabismus. Our data were similar to those of Steeves et al.
14 who investigated patients older than 8 years with early-onset strabismus.
Westall et al.
17 found no clear relation between stereopsis and OKN deficits. Wright
18 and Aiello et al.
19 examined three children who underwent unusual early surgery for esotropia at 3 and 4 months of age. Although these children eventually had normal stereoacuity, they had asymmetrical OKN. In contrast to these findings, van Hof-van Duin et al.
20 measured OKN in six normal, six stereodeficient, and six stereoblind subjects. OKN was clearly asymmetric in patients with no stereovision, but symmetric in subjects with rudimentary stereovision. This is in agreement with our study. Patients with PB in our study had peripheral fusion and/or stereopsis, but central scotomas in the nondominant eye when tested binocularly with the Bagolini test. They had small squint angles, which should easily be fused if normal potential of fusion is present. Therefore, it is likely that PB patients have inability of central fusion and small squint from birth. The lack of OKN asymmetries in the PB group argues, therefore, against the notion that OKN asymmetries are mainly dependent on the age of onset of squint. In monocularly deprived patients, OKN asymmetry is more pronounced if the deprivation is less profound,
26 because of more interocular rivalry. Peripheral fusion may reduce rivalry between eyes in PB and prevent development of asymmetric OKN.
In the PB group, the OKN gain was consistently lower for TN and NT stimulation for dominant and nondominant eyes, whereas the GB group had a normal OKN gain. This difference in the PB group increased with increasing stimulus velocity (significant for 60 deg/s). Van Hof-van Duin et al.
20 observed similar findings in a small group of patients. Reduced OKN gains in the PB group cannot be attributed to amblyopia, because they were also reduced in dominant and nondominant eyes and visual acuities of the nondominant eyes were similar to those in the NB group, who showed normal TN gains. We have found that young children, 1 to 2 years of age, with normal visual and binocular development, have reduced but symmetrical OKN gain for TN as well as NT stimulation, when compared with 20- to 40-year-old subjects (Valmaggia C, unpublished observations, 2002). Possibly in PB with microstrabismus, binocular cortical connections are sufficient for development of monocular OKN symmetry, but remain incomplete, preventing full OKN maturation to adult levels. In the cat, cortical projections provide for binocularity in approximately 40% of cells in the NOT, and are necessary for optokinetic responses for high stimulus velocities.
27 This could explain why gains were affected more at higher velocities in our subjects, with differences being significant only at 60 deg/s.
Visual acuities, measured at the time of strabismus detection or at the time of OKN measurement, were not correlated to OKN asymmetries. At the time of OKN measurement, most of our patients had relatively good visual acuity, some after occlusion therapy.
Patients in the GB group had the potential of stereovision, but had strabismus associated with diplopia, or signs of diplopia. Their mean OKN gain was similar to normal subjects. The only difference was that more subjects had an asymmetry factor out of normal range favoring either TN or NT stimulation. Larger OKN variability reflects a less precise OKN generation in the GB group. This may be associated with a less robust binocular system, causing sudden onset of strabismus at a later age, although binocular vision has developed.
In conclusion, our study shows that OKN gain and asymmetry are associated with the development of binocular vision. OKN investigation may be helpful to identify patients with binocularity or binocular potential in strabismus.
Submitted for publication March 28, 2003; revised July 13, 2003; accepted August 5, 2003.
Disclosure:
C. Valmaggia, None;
F. Proudlock, None;
I. Gottlob, None
The publication costs of this article were defrayed in part by page charge payment. This article must therefore be marked “
advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Corresponding author: Christophe Valmaggia, Department of Ophthalmology, Kantonsspital, CH-9007 St. Gallen, Switzerland;
[email protected].
Table 1. Details of Patients with No Measurable Binocularity
Table 1. Details of Patients with No Measurable Binocularity
| Patient | Age at Diagnosis (mo) | First Measured VA (DE) | First Measured VA (NDE) | Strabismus Form at Presentation | SA at Presentation (Degrees) | DVD | Occlusion Therapy | Age at OKN Test (y) | VA at Time of OKN Test (DE) | VA at Time of OKN Test (NDE) | Strabismus Form at Time of OKN Test | SA at Time of OKN Test (Degrees) |
| 1 | 14 | 0.8 | 0.6 | R eso | 11.4 | N | Y | 9 | 1.0 | 1.0 | R exo | 8.0 |
| 2 | 18 | 0.8 | 0.6 | L exo | 11.4 | N | Y | 48 | 1.0 | 1.0 | L eso | 21.3 |
| 3 | 8 | 0.6 | 0.8 | R eso | 16.7 | Y | Y | 7 | 1.0 | 0.6 | R exo | 1.2 |
| 4 | 5 | 1.25 | 1.0 | L exo | 22.3 | N | N | 33 | 1.25 | 0.8 | L exo | 8.0 |
| 5 | 3 | 0.5 | 0.4 | L eso | 19.3 | Y | Y | 11 | 1.0 | 1.0 | L eso | 21.3 |
| 6 | 16 | 0.6 | 0.4 | R eso | 19.3 | N | Y | 40 | 1.25 | 1.0 | R exo | 8.0 |
| 7 | 4 | 0.8 | 0.6 | L eso | 11.4 | Y | Y | 37 | 0.9 | 1.0 | L exo | 6.3 |
| 8 | 2 | 0.8 | 0.3 | R eso | 19.3 | Y | Y | 14 | 1.0 | 0.6 | R eso | 12.5 |
| 9 | 4 | 1.25 | 0.1 | L eso | 19.3 | Y | Y | 10 | 0.9 | 0.8 | L eso | 22.3 |
| 10 | 6 | 0.5 | 0.4 | L eso | 14.1 | Y | Y | 13 | 1.0 | 0.9 | L eso | 8.0 |
| 11 | 12 | 1.0 | 0.8 | L eso | 23.4 | N | N | 14 | 1.0 | 1.25 | L eso | 7.0 |
| 12 | 18 | 1.25 | 1.0 | R exo | 14.1 | Y | N | 9 | 1.0 | 1.0 | R exo | 12.5 |
| 13 | 2 | 0.6 | 0.6 | R eso | 24.0 | Y | Y | 6 | 0.9 | 0.7 | R exo | 12.5 |
| 14 | 3 | 1.0 | 0.8 | L exo | 9.1 | Y | Y | 10 | 1.0 | 0.9 | L exo | 2.3 |
| 15 | 2 | 0.8 | 0.5 | R eso | 24.0 | N | Y | 36 | 0.6 | 0.6 | R eso | 20.0 |
| 16 | 1 | 0.5 | 0.3 | L eso | 40.0 | Y | Y | 5 | 0.9 | 0.6 | L eso | 12.5 |
| 17 | 5 | 0.6 | 0.5 | R eso | 19.3 | N | Y | 9 | 0.9 | 0.8 | R eso | 12.5 |
| 18 | 12 | 0.5 | 0.1 | R eso | 22.0 | Y | Y | 9 | 0.6 | 0.6 | R eso | 21.8 |
| 19 | 16 | 1.0 | 0.5 | R eso | 19.3 | N | Y | 8 | 1.0 | 0.8 | R eso | 15.7 |
| 20 | 1 | 1.0 | 0.4 | L exo | 14.1 | Y | N | 22 | 1.0 | 1.0 | L eso | 12.5 |
Table 2. Details of Patients with Poor Binocularity
Table 2. Details of Patients with Poor Binocularity
| Patient | Age at Diagnosis (mo) | First Measured VA (DE) | First Measured VA (NDE) | Strabismus Form at Presentation | SA at Presentation (Degrees) | Occlusion Therapy | Surgery | Age at OKN Test (y) | VA at Time of OKN Test (DE) | VA at Time of OKN Test (NDE) | Strabismus Form at Time of OKN Test | SA at Time of OKN Test (Degrees) | Titmus Fly |
| 1 | 46 | 1.25 | 0.1 | R eso | 4.6 | Y | N | 7 | 1.0 | 0.8 | R eso | 4.6 | Pos |
| 2 | 44 | 1.25 | 0.8 | R exo | 19.3 | Y | Y | 8 | 1.0 | 0.8 | R exo | 3.5 | Pos |
| 3 | 56 | 1.25 | 1.0 | L eso | 16.7 | N | Y | 12 | 1.0 | 1.0 | L eso | 4.6 | Neg |
| 4 | 73 | 1.0 | 1.0 | L eso | 23.8 | N | Y | 14 | 1.0 | 1.0 | L eso | 4.6 | Neg |
| 5 | 56 | 0.8 | 1.25 | L eso | 19.3 | N | Y | 9 | 1.0 | 1.0 | L eso | 4.6 | Pos |
| 6 | 66 | 1.0 | 0.6 | R eso | 16.7 | Y | Y | 12 | 1.0 | 1.0 | R eso | 3.5 | Pos |
| 7 | 64 | 1.0 | 0.5 | R eso | 4.5 | Y | N | 11 | 1.0 | 1.0 | R eso | 4.6 | Neg |
| 8 | 54 | 1.25 | 0.5 | L eso | 4.5 | N | N | 12 | 1.25 | 0.6 | L eso | 0.6 | Pos |
| 9 | 48 | 1.25 | 1.25 | R eso | 14.1 | N | Y | 9 | 1.25 | 1.25 | R eso | 4.6 | Pos |
| 10 | 51 | 0.9 | 0.4 | L eso | 16.3 | Y | Y | 8 | 1.0 | 1.0 | L eso | 2.3 | Neg |
| 11 | 43 | 1.2 | 0.2 | L eso | 4.5 | Y | N | 13 | 1.0 | 0.6 | L eso | 2.3 | Pos |
| 12 | 43 | 1.25 | 0.6 | R eso | 16.7 | N | Y | 20 | 1.0 | 1.0 | R eso | 4.6 | Pos |
| 13 | 67 | 0.8 | 0.6 | L eso | 5.0 | Y | N | 8 | 0.8 | 0.8 | L eso | 4.6 | Pos |
| 14 | 82 | 0.9 | 0.2 | R eso | 16.7 | N | Y | 54 | 1.0 | 0.8 | R eso | 2.3 | Pos |
| 15 | 34 | 1.0 | 0.5 | R eso | 4.6 | Y | N | 10 | 1.0 | 0.6 | R eso | 4.6 | Pos |
| 16 | 67 | 1.0 | 0.5 | R eso | 4.6 | N | N | 5 | 1.0 | 1.0 | R eso | 1.2 | Neg |
| 17 | 81 | 0.6 | 1.0 | L eso | 3.5 | N | N | 37 | 1.0 | 0.6 | L eso | 3.5 | Pos |
| 18 | 34 | 1.25 | 1.0 | R eso | 23.8 | N | Y | 50 | 1.0 | 0.6 | R eso | 4.6 | Pos |
| 19 | 43 | 1.0 | 0.1 | L eso | 2.0 | Y | N | 6 | 1.0 | 0.6 | L exo | 0.6 | Pos |
| 20 | 89 | 1.0 | 0.5 | L eso | 4.6 | Y | N | 7 | 0.8 | 0.8 | L eso | 3.2 | Pos |
Table 3. Details of Patients with Good Binocularity
Table 3. Details of Patients with Good Binocularity
| Patient | Age at Diagnosis (mo) | First Measured VA (DE) | First Measured VA (NDE) | Strabismus Form at Presentation | SA at Presentation (Degrees) | Occlusion Therapy | Age at OKN Test (y) | VA at Time of OKN Test (DE) | VA at Time of OKN Test (NDE) | Stereoacuity TNO Test (seconds of arc) |
| 1 | 24 | 1.00 | 1.00 | R eso | 19.3 | Y | 6 | 1.00 | 1.00 | 240 |
| 2 | 32 | 0.50 | 0.50 | L eso | 21.9 | Y | 11 | 1.00 | 1.00 | 60 |
| 3 | 28 | 1.25 | 1.25 | R eso | 20.9 | N | 14 | 1.00 | 1.00 | 120 |
| 4 | 36 | 0.80 | 0.80 | R eso | 15.2 | N | 10 | 1.25 | 1.25 | 60 |
| 5 | 19 | 1.00 | 1.00 | Alt eso | 26.7 | N | 8 | 1.00 | 1.00 | 60 |
| 6 | 35 | 0.30 | 0.30 | L eso | 15.2 | N | 6 | 1.00 | 1.00 | 120 |
| 7 | 27 | 0.90 | 0.90 | R eso | 19.3 | N | 6 | 1.25 | 1.25 | 240 |
| 8 | 36 | 0.80 | 1.00 | R eso | 16.7 | N | 16 | 1.25 | 1.25 | 60 |
| 9 | 29 | 0.80 | 0.80 | L eso | 19.3 | N | 10 | 0.90 | 1.00 | 240 |
| 10 | 18 | 1.00 | 1.00 | Alt eso | 28.0 | N | 11 | 1.25 | 1.25 | 60 |
| 11 | 32 | 0.63 | 0.63 | Alt eso | 15.2 | N | 6 | 1.25 | 1.25 | 60 |
| 12 | 27 | 0.90 | 0.90 | Alt eso | 16.7 | N | 12 | 1.00 | 1.00 | 120 |
| 13 | 22 | 0.80 | 1.0 | Alt eso | 19.3 | N | 14 | 1.00 | 1.00 | 60 |
| 14 | 29 | 0.50 | 0.50 | R eso | 20.0 | N | 9 | 0.90 | 1.00 | 60 |
| 15 | 34 | 0.80 | 0.80 | R eso | 16.7 | N | 13 | 0.90 | 1.00 | 15 |
Table 4. The Percentage of Patients with OKN Gain Below Normal 95% Confidence Interval
Table 4. The Percentage of Patients with OKN Gain Below Normal 95% Confidence Interval
| TN (deg/s) | | | | NT (deg/s) | | | |
| 15 | 30 | 45 | 60 | 15 | 30 | 45 | 60 |
| No binocularity | | | | | | | | |
| DE | 0.0 | 5.0 | 10.0 | 0.0 | 60.0 | 55.0 | 60.0 | 60.0 |
| NDE | 0.0 | 0.0 | 0.0 | 0.0 | 80.0 | 60.0 | 70.0 | 55.0 |
| Poor binocularity | | | | | | | | |
| DE | 5.0 | 10.0 | 20.0 | 10.0 | 25.0 | 10.0 | 10.0 | 5.0 |
| NDE | 15.0 | 20.0 | 25.0 | 10.0 | 25.0 | 25.0 | 15.0 | 20.0 |
| Good binocularity | | | | | | | | |
| DE | 0.0 | 0.0 | 13.3 | 0.0 | 13.3 | 0.0 | 6.7 | 0.0 |
| NDE | 6.7 | 0.0 | 6.7 | 0.0 | 0.0 | 0.0 | 6.7 | 0.0 |
Table 5. The Percentage of Patients with Asymmetric OKN
Table 5. The Percentage of Patients with Asymmetric OKN
| TN>NT (deg/s) | | | | NT>TN (deg/s) | | | |
| 15 | 30 | 45 | 60 | 15 | 30 | 45 | 60 |
| No binocularity | | | | | | | | |
| DE | 65.0 | 55.0 | 50.0 | 55.0 | 0.0 | 0.0 | 5.0 | 10.0 |
| NDE | 80.0 | 85.0 | 75.0 | 80.0 | 0.0 | 0.0 | 0.0 | 0.0 |
| Poor binocularity | | | | | | | | |
| DE | 15.0 | 5.0 | 5.0 | 5.0 | 0.0 | 0.0 | 5.0 | 25.0 |
| NDE | 20.0 | 30.0 | 10.0 | 25.0 | 10.0 | 10.0 | 5.0 | 25.0 |
| Good binocularity | | | | | | | | |
| DE | 33.3 | 13.3 | 6.7 | 6.7 | 13.3 | 26.7 | 6.7 | 26.7 |
| NDE | 26.7 | 20.0 | 6.7 | 20.0 | 20.0 | 6.7 | 6.7 | 26.7 |
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