Abstract
Central disruption of fusion refers to a subject’s inability to align images, resulting in constant diplopia. Severely reduced vergences, or vergence anomalies, producing markedly decreased fusional amplitudes resembling fusional disruption have not been reported previously with convergence insufficiency. We report 3 patients with severe vergence anomaly in the setting of convergence insufficiency.
Convergence insufficiency is the inability to converge at near, resulting in asthenopia and diplopia. Patients demonstrate reduced near point of convergence (NPC), exodeviation at near greater than distance, and possibly reduced fusional convergence amplitudes.1 To our knowledge, convergence insufficiency has not been reported to cause near complete loss of sensory and motor fusion. We report 3 patients who presented at the pediatric ophthalmology clinic, Stanford University, with severe convergence insufficiency and inability to maintain or sustain fusion at near and distance. Through orthoptic treatment, 2 patients achieved reversal of their vergence anomalies.
Case Reports
Case 1
A healthy 12-year-old girl with history of convergence insufficiency presented with constant diplopia of 2 years’ duration. She had worsening symptoms despite multiple evaluations and convergence treatments. She denied prior injuries, and previous magnetic resonance imaging (MRI) of her brain was normal. Her visual acuity was 20/20 and J1+ in each eye. Cycloplegic refraction was –0.50 D in the right eye and –0.25 D in the left eye. She had a comitant left exotropia of 14Δ at distance, 25Δ at near, remote NPC, and decreased accommodation via Royal Air Force ruler. She had no fusion with Worth lights or Bagolini lenses; images were almost superimposed with 16Δ base-in at distance and 30Δ base-in at near but would immediately split. Torsion was considered noncontributory, because there was no oblique muscle abnormality, and prisms could align her diplopia. Treatment included Fresnel prisms that superimposed images: 15Δ base-in over the right eye and 2Δ base-in over the left eye for her distance spectacles (−0.75 D, both eyes) and 30Δ base-in over the right eye for near readers (+1.25 D, both eyes). She was instructed to wear prisms consistently and to practice attaining and maintaining fusion as much as possible. After 6 weeks, she was asymptomatic. Examination without prisms or glasses showed an exophoria of 4Δ at distance, 2Δ esophoria to 10Δ exophoria at near, normal NPC and accommodation, and resolution of fusional disruption with normal range of amplitudes. After 15 months, she remained asymptomatic, with continued improvement (4Δ exophoria at distance and 6Δ esophoria to 2Δ exophoria at near).
Case 2
A healthy 10-year-old boy presented with constant diplopia of 2 years’ duration. He denied prior injuries or spectacle use. On examination, his visual acuity was 20/15 in the right eye and 20/20 in the left eye, and J1+ in each eye. Cycloplegic refraction was +0.50 D in each eye. He had a comitant right exotropia 10Δ at distance, 30Δ at near, remote NPC, and normal accommodation. He could sensory fuse with 8Δ base-in at distance with no range and had only fleeting fusion/superimposition with 18Δ base-in at near. For reasons similar to those in case 1, torsion was considered noncontributory. Treatment included overminus glasses (–1.00 D, both eyes) to stimulate accommodative convergence with 8Δ base-in Fresnel prism over the left eye, jump convergence exercises, and fusion practice as much as possible. After 7 weeks, although he wore 8Δ base-in over both eyes, he showed improvement. Examination with 16Δ base-in prisms demonstrated exophoria of 8Δ at distance and maintenance of fusion at distance and near with a small range of amplitudes. Given the tentative fusion, he was instructed to continue using 8Δ base-in over both eyes and to begin remote convergence exercises. Because he improved with treatment, decision was made to defer brain MRI. After 7 weeks, he had resolution of diplopia and improved convergence and fusional reserves. Examination wearing his prism correction showed 6Δ exophoria at distance and near, 8Δ base-out positive fusional reserve at distance, and 25Δ base-out positive fusional reserve at near. He was instructed to wear 8Δ base-in over the left eye only. After 4 months, he remained asymptomatic. Examination without his prismatic correction showed exophoria 16Δ at distance, intermittent exotropia 18Δ at near, normal NPC, and maintenance of fusion with normal range of amplitudes. Examination wearing 8Δ base-in prism showed exophoria of 6Δ at near. He continued wearing 8Δ base-in for near, slowly reducing frequency, then stopping. He demonstrated restoration of fusional disruption without prisms and normal convergence, though with slightly reduced fusional reserves. At 16 months’ follow-up, findings were stable.
Case 3
A healthy 11-year old boy with history of convergence insufficiency presented with constant diplopia for several years. He denied previous intracranial injury or spectacle use. His visual acuity was 20/40 in the right eye and 20/50 in the left eye. Cycloplegic refraction was +0.25 +0.25 ×165 D in the right eye and plano +0.25 ×160 D in the left eye. On examination, he had varying exotropia of 2Δ to esotropia of 2Δ at distance, alternating exotropia 14Δ at near, and remote NPC. He may have been overaccommodating to stimulate fusion with accommodative convergence, as evidenced by his reduced vision and varying deviation from esotropia to exotropia at distance. He was instructed to perform remote convergence exercises and order glasses for prisms. Two weeks later, he had not obtained glasses and had barely performed the exercises, with minimal improvement. He had alternating exotropia 1Δ with varying responses of diplopia, sensory fusion, left suppression at distance, and right exotropia of 8Δ−10Δ at near with diplopia. After much concentration, he fused momentarily with 8Δ−10Δ base-in. In this case too, and for similar reasons, torsion was considered noncontributory. He was instructed to wear 8Δ base-in Fresnel prism over his left eye during reading and do convergence exercises. He did not return for follow-up.
Discussion
Central disruption of fusion refers to a patient’s inability to align images, resulting in constant diplopia.2 Acquired loss of fusion is often associated with severe head trauma and midbrain injury, intracranial lesions, or chronic unilateral sensory deprivation.3 Although spontaneous resolution of fusional disruption can occur,4,5 prognosis is guarded due to intractable diplopia.3 We describe convergence insufficiency associated with severely reduced vergences, resulting in near complete loss of sensorimotor fusion with refractory diplopia. Recognition of this entity is necessary to initiate treatment, including prismatic correction and concerted effort to superimpose images as much as possible, orthoptic exercises to strengthen motor fusion, and gradual weaning of prisms as fusional capabilities improve. With nonsurgical management, 2 patients regained fusion. The third patient had not improved on final follow-up. Recognition of severely reduced vergences associated with convergence insufficiency is paramount to counsel these patients and appropriately initiate treatment to reverse disruption of binocularity.
Literature Search
PubMed was searched on April 1, 2020 without date restriction, for English-language results, using the following terms: central fusional disruption, convergence insufficiency, fusion disruption, and loss of fusion.
Acknowledgments
This study was supported by a core grant from the National Institutes of Health (P30 EY026877) and by an unrestricted grant from Research to Prevent Blindness Inc to the Department of Ophthalmology, Stanford University.
Footnotes
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
References
- 1.Convergence Insufficiency Treatment Trial (CITT) Study Group. The convergence insufficiency treatment trial: design, methods, and baseline data. Ophthalmic Epidemiol 2008;15:24–36. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Lee MC. Acquired central fusional disruption with spontaneous recovery. Strabismus 1998;6:175–9. [DOI] [PubMed] [Google Scholar]
- 3.Pratt-Johnson JA, Tillson G. Acquired central disruption of fusional amplitude. Ophthalmology 1979;86:2140–42. [DOI] [PubMed] [Google Scholar]
- 4.Digout LG, Awad AH. Restoration of binocular single vision after long-term fusion disruption. J AAPOS 2003;7:185–9. [DOI] [PubMed] [Google Scholar]
- 5.Pratt-Johnson JA. Fusion ability lost and regained in visual adults. Graefes Arch Clin Exp Ophthalmol 1988;226:111–12. [DOI] [PubMed] [Google Scholar]
