a_review_of_ci

A Review of ConvergenceInsufficiency: What Are WeReally Accomplishing withExercises?

Kyle Arnoldi, C.O., C.O.M.T.James D. Reynolds, M.D.

CONVERGENCE INSUFFICIENCY:DEFINITION AND ETIOLOGY

Convergence insufficiency (CI) is an un-common disorder of ocular motility char-

acterized by an inadequate amount of ocu-lar convergence needed to achieve andmaintain comfortable, clear, single binocu-lar vision at near fixation. Exodeviationsare found in 1% of the general population,1

American Orthoptic Journal 123

© 2007 Board of Regents of the University of Wisconsin System, American Orthoptic Journal, Volume 57, 2007, ISSN 0065-955X, E-ISSN 1553-4448

ABSTRACT

Introduction: Orthoptic exercises have been the primary treatment for convergence insufficiencysince this condition’s first description in 1855. It is presumed that exercises work by improving fu-sional convergence. In recent years, research from eye movement laboratories has challenged ourtheories on the nature and dynamics of convergence, the effect of convergence exercises, and the eti-ology of primary convergence insufficiency.

Methods: A review of the ophthalmological, optometric, and basic science literature was done to re-trieve the most recent research on vergence eye movements and convergence insufficiency.

Results: Convergence appears to be a bi-phasic response to a change in stimulus position in depth.The first phase, which may represent the contribution of proximal convergence, is not under visualfeedback, is fast with a short latency, and is triggered by stimuli moving rapidly in depth or by large,sudden changes in fixation. This phase is followed by a slow vergence movement with a slightly longerlatency, triggered by small disparity vergence errors. The second phase is under the control of visualfeedback, and represents the contributions of fusional and accommodative convergence. Eye movementrecordings indicate that the velocity and amplitude of the first phase of convergence are temporarilyadaptable with exercises. The second phase does not appear to be amenable to training. Tonic con-vergence is also trainable.

Conclusion: Convergence exercises are effective in temporarily improving the dynamics of proximaland tonic convergence, but have little effect on fusional or accommodative convergence.

From the State University of New York at Buffalo, Buffalo, New York.

Requests for reprints should be addressed to: Kyle Arnoldi, C.O., C.O.M.T., University Ophthalmology Services, 3580 SheridanDr., Suite 140, Amherst, NY 14226; [email protected]

This research was supported in part by a Challenge Grant to the Department of Ophthalmology from the Research to PreventBlindness, Inc., New York, NY.

and CI accounts for 11% to 19% of childrenwith an exodeviation.2,3 Based on these fig-ures, the prevalence of CI in the generalpopulation can be estimated at approxi-mately 0.1% to 0.2%. Govindan and co-workers found an incidence of 64 new casesper year, per 100,000 patients aged 19years and younger.2

CI may be caused by or associated withhead trauma,4–10 neurodegenerative dis-eases,11–13 ischemia,14–16 thyroid ophthal-mopathy,17 myasthenia gravis,17 toxicagents or medications,4,11,18 infection orinflammation,11,19 or decompression sick-ness.20 CI is most commonly a primary con-dition, typically presenting in the youngadult population, and presumably causedby an inborn deficiency or acquired imbal-ance of vergence eye movements that hasyet to be identified.21–23

DIAGNOSTIC CRITERIA

The most common clinical signs of CI asreported in the literature are a remote nearpoint of convergence (typically beyond 10cm from the bridge of the nose),9,21–27 andpoor convergence amplitudes (a breakpoint ≤ 15Δ, with recovery more than 4Δ

from the break point).23,25,26,28 Other signsreported to be associated with CI includean exodeviation at near fixation ≥ 10Δ,29–31

a low AC/A ratio (≤ 2:1),21,29,31 and poorvergence “facility” (ease with which ver-gence is generated and the movement com-pleted).23,26,32 Some authors claim thatdecreased accommodative amplitudes forage,21,25,31,33 and poor accommodative “fa-cility”32 are also associated with the condi-tion.

Symptoms associated with convergenceinsufficiency include fatigue, blurred visionat near, intermittent diplopia at near, “eyestrain,” tension in and around the eyes,and the sensation of the print moving whilereading. Convergence insufficiency is anuncommon cause of headaches, accountingfor less than 1% of all headaches present-

ing to the ophthalmologist.34 Among pub-lished clinical studies, the presence ofsymptoms is the single most common cri-terion used to diagnose CI, to monitor prog-ress of the condition, or to determine thesuccess of its treatment.31

TREATMENT OPTIONS

CI was first described by von Graefe in1855, who recommended exercises to im-prove convergence amplitudes.22 Suchexercises continue to be the mainstay of treatment to this day. A wide variety ofoffice-based and home-based orthoptic ex-ercises have been designed to reduce symp-toms of CI. It has been hypothesized thatexercises work because they improve fu-sional convergence and/or modify accom-modative convergence to allow comfortablenear binocular vision. Many patients havefound temporary relief with these methods,whether or not the clinical signs or mea-surements have significantly improved.25,35

However, spontaneous improvement insymptoms has also been reported,4,30,36,37

and one can not ignore the potential for aplacebo effect, particularly if the main out-come criterion is improvement in symp-toms, as is often the case.

Convergence has been studied in severaleye movement laboratories in recent years,in order to more accurately quantify nor-mal and abnormal vergence and accommo-dation. These studies have discovered newintricacies to normal convergence, and re-vealed the vergence characteristics thatare susceptible to adaptation with exer-cises.

DYNAMICS OF NORMALCONVERGENCE

As with all types of eye movements, ver-gence is described and defined in terms oflatency, velocity, amplitude, and the stim-ulus needed to generate the response. La-tency is the length of time between the

CONVERGENCE INSUFFICIENCY

124 Volume 57, 2007

presentation of the stimulus and the onsetof the response. Latency is a function ofcentral nervous system processing time,and is a measure of the efficiency of initia-tion of the eye movement (reaction time).The mean latency of the vergence responsein adults is approximately 160 to 180 msec,compared to approximately 316 msec forchildren.38–40 Though significantly longerin children, latencies approach adult lev-els by age ten years. Yang and co-workersreported that the improvement with age isthe result of attention factors and thevisuomotor process alone.39 Latency is sim-ilar under monocular and binocular condi-tions.40

Vergence is considered one of the “slow”eye movements, with pure vergence peakvelocity measured at 30–80° per second.27

Velocity is faster for sudden, large changesin fixation distance, and under binocularconditions.40–41 Both velocity and latencyare important components of vergence fa-cility.

The amplitude of an eye movement is of-ten described in terms of gain. Gain is ameasure of how closely the responsematches the change in stimulus. Vergencegain is higher under binocular conditionsthan under monocular conditions,40 due tothe input of disparity-driven convergence.The maximum degree of disparity that willevoke a vergence response is approxi-mately 4° of arc.42

Convergence movements can be dividedinto two general categories based on func-tion: those that serve to grossly align theeyes in the awake state (tonic vergence),and those that serve to keep the object ofregard imaged onto both foveas withchanges in object position in depth (proxi-mal, fusional, and accommodative conver-gence). Tonic vergence represents the base-line, resting level of vergence tone. Tonicvergence can be observed by comparing eyeposition while asleep with eye positionwhile awake but in the absence of other vi-sual cues.

The latter group of convergence move-ments can be further subdivided based onthe stimulus required to generate a re-sponse. Awareness of a near object triggersproximal convergence, binocular image dis-parity triggers fusional convergence, andretinal image blur triggers accommodativeconvergence. Each of these subtypes of con-vergence differs slightly in latency, veloc-ity, and amplitude as well.

Under normal conditions, proximal, fu-sional, and accommodative convergencesrarely function in isolation. Laboratorystudies have shown how they coordinate toachieve the normal convergence responseto a change in stimulus position in depth.Convergence appears to be a bi-phasic re-sponse consisting of a “pulse” followed by a“step”.38,43,44 The vergence pulse initiatesthe movement and is open-looped,43 mean-ing that it is not under the control of visualfeedback. This phase is triggered by targetsmoving rapidly in depth, or by large, sud-den changes in fixation distance.38,42,44 Thepulse has a shorter latency, and a faster ve-locity than the step part of the response.38,40

In their work on proximal convergence,Wick and Bedell41,45 and Schor and co-workers44 concluded that proximal ver-gence most likely initiates the vergence re-sponse to changes in fixation from distantto near targets. Proximal convergence hasbeen found to account for 70–80% of thevergence response, with its contribution in-creasing with the onset of presbyopia.26,45,47

In addition, the dynamics of proximal con-vergence (velocity, latency) mimic thosefound in the initial phase of the conver-gence response.41–42 It is possible then thatthe initial, open-loop phase of the conver-gence response is the role of proximal con-vergence.

The step is closed-loop, modulated by vi-sual feedback, and is designed to completeand refine the vergence response.38,44 It istriggered by targets moving slowly indepth, or by small errors in image dispar-ity, and likely represents the contributions

ARNOLDI


of fusional convergence (primarily), and ac-commodative convergence (minimally).40

The step latency is longer by approxi-mately 60 msec (for fusional convergence)or more (for accommodative convergence),46

and the velocity is slower than for the ver-gence pulse.41 Figure 1 illustrates how thetypes of convergence may interact toachieve a normal convergence response.

ANATOMY OF THE VERGENCESIGNAL

Anatomical evidence of a two-step con-vergence response has been found in ani-mal studies. It has long been known thatthe midbrain reticular formation containsconvergence cells that fire just before andduring fusional or accommodative conver-gence.48–51 Their firing activity correlateswith vergence velocity and amplitude.More recently, the role of specific areas inthe pons has been clarified with respect tovergence. Omnipause neurons located inthe nucleus raphe interpositus in the ponsslow firing activity just before a fast ver-gence movement (vergence pulse),52–53

while cells in the nucleus reticularis teg-menti pontis are active during slow ver-gence (vergence step).54 These two groupsof pontine nuclei project to different areasof the cerebellum.53–54 There is also evi-dence of an internal representation of view-ing distance, independent of cues from ac-commodation caused by retinal image blur,that may be the anatomic substrate of theproximal component of the vergence re-sponse.53

CHARACTERISTICS OFCONVERGENCE SUSCEPTIBLE TOADAPTATION

Using a scleral search coil technique,Van Leeuwen and co-authors proved thatorthoptic training improved overall ver-gence amplitude, accuracy, and velocity inpatients with convergence insufficiency.57

The question is: which part(s) of the con-vergence response improved with orthop-tics? It has often been presumed thatorthoptic therapy is effective in treat-ing convergence insufficiency because itimproves fusional convergence ampli-


126 Volume 57, 2007

FIGURE 1: Graphic representation of a typical vergence response to a change instimulus position in depth. Convergence to a near target is bi-phasic. The initialresponse to a change in stimulus position is provided by proximal convergence.Fusional convergence is slower, with a longer latency.

-1

0

1

2

3

4

5

6

7

8

9

-0.25 0 0.25 0.5 0.75 1 1.25 1.5

Time (sec)

Ver

gen

ce (

P.D

.)

Total Response Fusional Proximal Stimulus

tudes.26,55–56 However, this assumption doesnot hold up in the face of results of recentlaboratory studies.

Several laboratories have reported thatthe velocity and amplitude of the initial,open-loop response is trainable with repe-tition, though the effect is not lasting.38,43,46

Latency appears to be consistent and nottrainable in normal subjects.43 In contrast,the velocity and amplitude of the secondphase of the convergence response does notappear to adapt with training.46,58 This sug-gests that it is not disparity or accom-modative convergence that improves withorthoptic exercises, as these types of con-vergence run on a closed-loop feedbacksystem. Figure 2 illustrates the effect oftraining on the convergence response to achange in stimulus location in depth thatwould require a convergence response of 8Δ to maintain the image on both foveae.The fusional convergence response is un-changed in latency, velocity, or amplitude.The proximal response, however, increases

in amplitude and velocity such that thetraining effect observed is an overshoot ofthe target position.

Tonic vergence also appears to beamenable to training. Several researchershave shown that sustained convergence ef-fort over a period of only minutes will tem-porarily shift tonic vergence inward. Thiseffect has been observed with sustainednear work46,58 and with prism adaptationusing base-out prism.40,59 Tonic vergenceadaptation is demonstrable in any agegroup, though the magnitude of the re-sponse declines with age at a rate of 0.6%per year.60

WHAT DOES THIS MEAN FOR THEMANAGEMENT OF CONVERGENCEINSUFFICIENCY?

Interpretation of the data suggests thatthe most effective exercises for convergenceinsufficiency would use either sustainedconvergence effort to improve tonic con-

ARNOLDI


FIGURE 2: Vergence response following training using an 8Δ change in stimulusposition. With repetition of a vergence demand of 8Δ, the amplitude and velocityof the proximal convergence response increases, causing an over-shoot of the fix-ation target (arrow). The fusional convergence response is unchanged from base-line with practice.

-2

0

2

4

6

8

10

12

-0.25 0 0.25 0.5 0.75 1 1.25 1.5

Time (sec)

Ver

gen

ce (

P.D

.)

Total Response Fusional Proximal Stimulus

vergence, or repetitive, rapid, and largeamplitude changes in stimulus position indepth to improve proximal convergence.Fortunately, many of the exercises alreadyin common use and shown to be effectivealready employ such techniques.35 Ex-amples might include reading with base-out prism, “jump vergence” exercises usingbase-out prism, or vergence facility exer-cises requiring rapid switches in fixationfrom distance to near. Our current under-standing of CI suggests that it cannot becured with exercises. Because the trainingeffect is temporary,38,43,61 lasting relief ofsymptoms would only be achieved withdaily exercises over an indefinite period oftime.

The results of these recent laboratorystudies have also raised some interestingquestions regarding the etiology, diagnosis,and management of convergence insuffi-ciency. Is it possible that a defect in a spe-cific subtype of convergence is responsiblefor primary CI? Is there more than one typeof primary CI? And, if so, can we deviseclinical tests to distinguish between thetypes, as well as create effective treatmentstargeting the specific deficiency? Finally, awell-designed, prospective study is neededto determine the long-term efficacy of or-thoptic exercises on tonic and proximalconvergence.

REFERENCES

1. Rutstein RP, Corliss DA: The clinical course of in-termittent exotropia. Optom Vis Sci 2003; 80:644–649.

2. Govindan M, Mohney BG, Diehl NN, Burke JP:Incidence and types of childhood exotropia. Oph-thalmology 2005; 112: 104–108.

3. Mohney BG, Huffaker RK: Common forms ofchildhood exotropia. Ophthalmology 2003; 110:2093–2096.

4. Al-Qurainy IA: Convergence insufficiency andfailure of accommodation following midfacialtrauma. Br J Oral Maxillofac Surg 1995; 33: 71–75.

5. Buncic JR: Systemic and pharmacological effectson near vision. Am Orthopt J 1999; 49: 2–6.

6. Cohen M, Groswasser Z, Barchadski R, Appel A:Convergence insufficiency in brain-injured pa-tients. Brain Inj 1989; 3: 187–191.

7. Kowal L: Ophthalmic manifestations of head in-jury. Aust N Z J Ophthalmol 1992; 20: 35–40.

8. Krohel GB, Kristan RW, Simon JW, Barrows NA:Posttraumatic convergence insufficiency. AnnOphthalmol 1986; 18: 101–102.

9. Lepore FE: Disorders of ocular motility followinghead trauma. Arch Neurol 1995; 52: 924–926.

10. Spierer A, Huna R, Rechtman C, Lapidot D: Con-vergence insufficiency secondary to subduralhematoma. Am J Ophthalmol 1995; 120: 258–260.

11. Brown B: The convergence insufficiency mas-querade. Am Orthopt J 1990; 40: 94–97.

12. Biousse V, Skibell BC, Watts RL, Loupe DN,Drews-Botsch C, Newman NJ: Ophthalmologicfeatures of Parkinson’s disease. Neurology 2004;62: 177–180.

13. Racette BA, Gokden MS, Tychsen L, PerlmutterJS: Convergence insufficiency in idiopathicParkinson’s disease responsive to levodopa. Stra-bismus 1999; 7: 169–174.

14. Burde RM, Savino PJ, Trobe JD. Clinical Deci-sions in Neuro-Ophthalmology. St. Louis: Mosby;1985. pp. 170–171.

15. Ohtsuka K, Maekawa H, Takeda M, Uede N,Chiba S: Accommodation and convergence insuf-ficiency with left middle cerebral artery occlusion.Am J Ophthalmol 1988; 106: 60–64.

16. Ohtsuka K, Maekawa H, Sawa M: Convergenceparalysis after lesions of the cerebellar peduncles.Ophthalmologica 1993; 206: 143–148.

17. Bruke JP, Shipman TC, Watts MT: Convergenceinsufficiency in thyroid eye disease. J PediatrOphthalmol Strabismus 1993; 30: 127–129.

18. Tassinari J: Methyldopa-related convergence in-sufficiency. J Am Optom Assoc 1989; 60: 311–314.

19. Pickwell LD, Hampshire R: Convergence insuffi-ciency in patients taking medicines. OphthalmicPhysiol Opt 1984; 4: 151–154.

20. Lieppman ME: Accommodation and convergenceinsufficiency after decompression sickness. ArchOphthalmol 1981; 99: 453–456.

21. Bartiss MJ: Convergence insufficiency. www.emedicine.com. 2005.

22. von Noorden GK, Campos EC. Binocular Visionand Ocular Motility. 6th ed. St. Louis: Mosby;2002. pp. 502–504.

23. Wright KW. Pediatric Ophthalmology and Stra-bismus. St. Louis: Mosby; 1995. pp. 199–200.

24. Ansons AM, Davis H. Diagnosis and Managementof Ocular Motility Disorders. 3rd ed. Oxford:Blackwell Science; 2001. pp. 319–322.

25. Mazow ML, Musgrove K, Finkelman S: Acute ac-commodative and convergence insufficiency. AmOrthopt J 1991; 41: 102–109.


128 Volume 57, 2007

26. Cornell E, Predebon J, Vu YP: The effect of or-thoptic treatment on the proximal component ofthe near response. In: Pritchard C, ed. Orthopticsin Focus: Transactions of the IX InternationalOrthoptic Congress. Stockholm: 1999. pp. 123–126.

27. VanLeeuwen AF, Westen MJ, vanderSteen J, deFaber J-T HN, Collewijn H: Gaze-shift dynam-ics in subjects with and without symptoms of con-vergence insufficiency: influence of monocularpreference and the effect of training. Vision Res1999; 39: 3095–3107.

28. Jenkins RH: Characteristics and diagnosis ofconvergence insufficiency. Am Orthop J 1999; 49:7–11.

29. Rosenbaum AL, Santiago AP. Clinical StrabismusManagement. Philadelphia: WB Saunders; 1999.p. 165.

30. Scheiman M, Mitchell GL, Cotter S, Cooper J,Kulp M, Rouse M, Borsting E, London R,Wensveen J: A randomized clinical trial of treat-ments for convergence insufficiency in children.Arch Ophthalmol 2005; 123: 14–24.

31. Daum KM: Characteristics of convergence insuf-ficiency. Am J Optom Physiol Optics 1988; 65:426–438.

32. Gall R, Wick B: The symptomatic patient withnormal phorias at distance and near: What testsdetect a binocular vision problem? Optometry2003; 74: 309–322.

33. Rouse MW, Borsting E, DeLand PN: Reliabilityof binocular vision measurements used in theclassification of convergence insufficiency. OptomVis Sci 2002; 79: 254–264.

34. Kaimbo KD, Missotten L: Headaches in ophthal-mology. J Fr Ophtalmol 2003; 26: 143–147.

35. Rawstron JA, Burley CD, Elder MJ: A systematicreview of the applicability and efficacy of eye ex-ercises. J Pediatr Ophthalmol Strabismus 2005;42: 82–88.

36. Dragomir M, Trus L, Chirila D, Stingu C: Or-thoptic treatment efficiency in convergence in-sufficiency treatment. Oftalmologica 2001; 53:66–69.

37. Birnbaum MH, Soden R, Cohen AH: Efficacy ofvision therapy for convergence insufficiency in anadult male population. J Am Optom Assoc 1999;70: 225–232.

38. Munoz P, Semmlow JL, Yuan W, Alvarez TL:Short term modification of disparity vergence eyemovements. Vision Res 1999; 39: 1695–1705.

39. Yang Q, Bucci MP, Kapoula Z: The latency of sac-cades, vergence, and combined eye movements inchildren and adults. Invest Ophthalmol Vis Sci2002; 43: 2939–2949.

40. Cumming BG, Judge SJ: Disparity-induced andblur-induced convergence eye movement and ac-

commodation in the monkey. J Neurophysiol1986; 55: 896–914.

41. Wick B, Bedell HE: Rapid- and slow-velocity ver-gence eye movements. Ophthalmic Physiol Opt1992; 12: 420–424.

42. Erkelens CJ, Collewijn H: Eye movements in re-lation to loss and regaining of fusion of disjunc-tively moving random-dot stereograms. HumNeurobiol 1985; 4: 181–188.

43. Takagi M, Oyamada H, Abe H, Zee DS, HawebeH, Miki A, Usui T, Bando T: Adaptive changes indynamic properties of human disparity-inducedvergence. Invest Ophthalmol Vis Sci 2001; 42:1479–1486.

44. Schor CM, Alexander J, Cormack L, Stevenson S:Negative feedback control model of proximal con-vergence and accommodation. Ophthalmic Phys-iol Opt 1992; 12: 307–318.

45. Wick B, Bedell HE: Magnitude and velocity ofproximal vergence. Invest Ophthalmol Vis Sci1989; 30: 755–760.

46. Semmlow JL, Yuan W: Adaptive modification ofdisparity vergence components: An independentcomponent analysis study. Invest Ophthalmol VisSci 2002; 43: 2189–2195.

47. Wick B: Clinical factors in proximal vergence. AmJ Optom Physiol Opt 1985; 62: 1–18.

48. Mays LE: Neural control of vergence eye move-ments: Convergence and divergence neurons inthe midbrain. J Neurophysiol 1984; 51: 1091–1108.

49. Mays LE, Porter JD, Gamlin PD, Tello CA:Neural control of vergence eye movements: neu-rons encoding vergence velocity. J Neurophysiol1986; 56: 10007–10021.

50. Zhang Y, Mays LE, Gamlin PD: Characteristicsof near response cells projecting to the oculomotornucleus. J Neurophysiol 1992; 67: 944–960.

51. Judge SJ, Cumming BG: Neurons in the monkeymidbrain with activity related to vergence eyemovement and accommodation. J Neurophysiol1986; 55: 915–930.

52. Busettini C, Mays LE: Pontine omnipause activ-ity during conjugate and disconjugate eye move-ments in macaques. J Neurophysiol 2003; 90:3838–3853.

53. Mays LE, Gamlin PDR: Neuronal circuitry con-trolling the near response. Curr Opin Neurobiol1995; 5: 763–768.

54. Rambold H, Neumann G, Helmchen C: Vergencedeficits in pontine lesions. Neurology 2004; 62:1850–1853.

55. von Noorden GK, Campos EC. Binocular Visionand Ocular Motility. 6th ed. St. Louis: Mosby;2002. pp. 502–504.

56. Petrunak JL: The treatment of convergence in-sufficiency. Am Orthopt J 1999; 49: 12–16.

ARNOLDI


57. Van Leeuwen AF, deFaber JTHN, vanderSteen J:Vergence eye movements and asthenopia: Is ver-gence training useful? In: Advances in Strabis-mology. Lennerstrand G, ed. Buren, The Nether-lands: Aeolus Press; 1999. pp. 111–115.

58. Yuan W, Semmlow JL: The influence of repetitiveeye movements on vergence performance. VisionRes 2000; 40: 3089–3098.

59. Schor CM: Adaptive regulation of accommodativevergence and vergence accommodation. Am J Op-tom Physiol Opt 1986; 63: 587–609.

60. Winn B, Gillmartin B, Sculfor DL, Bamford JC:

Vergence adaptation and senescence. Optom VisSci 1994; 71: 797–800.

61. Deshpande SB, Ghosh RK: Study of primary con-vergence insufficiency. Indian J Ophthalmol1991; 39: 112–114.

Key words: convergence insufficiency,convergence amplitudes, proximal conver-gence, fusional convergence, accommoda-tive convergence


130 Volume 57, 2007

a_review_of_ci

Documents