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Acute Concomitant Esotropia of Adulthood

Abraham Spierer, MD

Purpose: To identify the characteristics of adult patients who develop acute concomitant esotropia ofadulthood.Design: Retrospective noncomparative case series.Participants: Ten patients were included in this study.Intervention: The charts of all adults with acute-onset concomitant esotropia who were examined at our

institute between 1990 and 1997 were reviewed, and those who had developed the syndrome when they wereolder than the age of 16 years were included in this study. All participants underwent a complete ocular andphysical examination, including brain and orbital computed tomography.

Main Outcome Measures: Angle of esotropia, measured by the prism and cover test.Results: The mean age standard deviation at the time of the ocular and physical examination was 38

18.6 years (range, 1870 years). The mean myopic error was 4.1 3.2 diopters (range, 2.0 to8.5 diopters).Nine of the 10 patients were myopic. The mean angle of esotropia was 33.8 14.7 prism diopters (range, 18 60prism diopters). The mean period of follow-up was 2.2 1.0 years (range, 1 4 years). After surgery, all patientswere orthophoric or minimally esophoric, and in all of them, stereoacuity (measured by the Titmus stereofly test)was 40 arc seconds.

Conclusions: In a well-defined group of adult patients with acute-onset concomitant esotropia, almost allwere myopic, and all regained normal stereopsis after surgery. Acute concomitant esotropia of adulthood shouldprobably be classified as a distinct subgroup of acute-onset esotropia. Ophthalmology 2003;110:10531056

2003 by the American Academy of Ophthalmology.

Late-onset esotropia is the term used to describe the onsetof esotropia with diplopia after infancy. According toBurian and Miller,1 acute or late-onset esotropia can bedivided into three categories: (1) Acute-onset concomitantstrabismus after occlusion (Swan type). This may be pre-

cipitated by occlusion of one eye or loss of vision in one eyein a patient with or without significant hypermetropia. (2)Concomitant convergent strabismus of the Franceschettitype. In this type of esotropia, there is a minimal amount ofhypermetropia. No underlying cause of the strabismus canbe found, although Bielschowsky2 attributed the acute onsetof the deviation in his patients to physical or psychic shockor exhaustion. Before onset of the strabismus, these patientsmay or may not have binocular vision. (3) Concomitantconvergent strabismus of the Bielschowsky type. Thesepatients are myopic (5 diopters) and exhibit a constantesodeviation at distance but not at near fixation. On presen-tation, the angle of deviation is usually small, but it in-creases gradually over time. Abduction may be slightlyrestricted in some cases, prompting Burian and Miller1 tosuggest that this type be identified with paralysis of diver-gence. The list of characteristics of the Bielschowsky typewas later modified3 to include higher degrees of myopia, as

well as constant and equal deviations at distance and nearfixation.

Since that early report, most of the articles published onacute- or late-onset esotropia have described series compris-ing both adults and children. The aim of this report was to

characterize the sudden onset of esotropia in adults, allow-ing us to define this condition as acute concomitant esotro-pia of adulthood.

Patients and Methods

The charts of all adults with acute-onset concomitant esotropiawho were examined at the Goldschleger Eye Institute, ShebaMedical Center, between 1990 and 1997 were reviewed. Patientswho met the following criteria were included in this retrospectivestudy: (1) a diagnosis of acute-onset concomitant esotropia (inconcomitant esotropia, the deviation, within physiologic limits, isthe same in all directions of gaze); (2) age 16 years at the timeof onset; (3) corrected visual acuity of 6/6 in both eyes; (4) nohistory of eye problems; (5) no cause of the interruption of fusion;and (6) no history of systemic disease or head trauma. None of thepatients had a family history of strabismus.

All ocular examinations, preoperative strabismus measure-ments, strabismus surgery, and postoperative strabismus measure-ments were performed by the same physician. Strabismus wasmeasured with the prism and cover test for near (30-cm) anddistance (6-m) fixation, as well as for all directions of gaze, withrefractive correction. The prism and cover test was performed byholding a cover in front of each eye alternately while the patientmaintained fixation. For esotropia, a base-out prism is used toneutralize the ocular movement, and esotropia is measured interms of the prism strength required to offset the movement. In all

Originally received: December 10, 2001.Accepted: October 31, 2002. Manuscript no. 211023.

Goldschleger Eye Institute, Sheba Medical Center, Tel-Hashomer, Israel;and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.

Reprint requests to Abraham Spierer, MD, Goldschleger Eye Institute,Sheba Medical Center, 52621 Tel-Hashomer, Israel. E-mail:[email protected]

1053 2003 by the American Academy of Ophthalmology ISSN 0161-6420/03/$see front matterPublished by Elsevier Science Inc. doi:10.1016/S0161-6420(03)00102-7

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measurements, an accommodative target was used. Cycloplegicrefraction was performed in all patients.

All patients in the study underwent a complete physical exam-ination, including brain and orbital computed tomography, and, insome cases, magnetic resonance imaging. All of the study partic-ipants underwent surgery, in which an adjustable suture techniquewas used. The type and amount of surgery are summarized in

Table 1. Where necessary, patients underwent postoperative ad-justment to orthophoria.

Results

Ten patients were found to have developed esotropia when theywere in their late teens or older and were included in this study. Inall of them, the esotropia had developed from 2 to 5 years beforetheir eye examination. The delay in presentation was attributable todelay on the part of either the referring physician or the patientsthemselves.

The age (mean standard deviation) of the patients at thetime of the eye examination was 38 18.6 years (range, 18 70years). Computed brain and orbital tomography (and magneticresonance imaging, where performed) were normal. The meanmyopic error was 4.1 3.2 diopters (range, 2.0 to 8.5diopters). Nine of the 10 patients had myopia, and in 6 of them,myopia was 4 diopters. Only one patient was hyperopic. Themean angle of esotropia was 33.8 14.7 prism diopters (range,18 60 prism diopters). The mean follow-up period was 2.2 1.0 years (range, 1 4 years). The patients data are summarizedin Table 1.

Each patient had a corrected visual acuity of 6/6 in both eyes.Anterior segment examination and funduscopy were normal ex-cept for mild myopic retinal changes seen in some patients. In eachpatient, the angles of esotropia were equal for distance and for near

fixation (differing by 5 prism diopters), and ocular ductions andvergences were normal.

All of the patients underwent surgery. After the operation, allwere found to be orthophoric or minimally esophoric, and in all ofthem, stereoacuity (measured by the Titmus stereofly test) was 40arc seconds.

Discussion

Three types of acute-onset esotropia have been described:the Swan type, which results from occlusion; the France-schetti type, which is associated with mild hyperopia; andthe Bielschowsky type, which is associated with myopia. Inspeculating on the role ofmyopia in the development of thissyndrome, Bielschowsky2 claims that uncorrected myopialeads to the development of increased tonus of the medialrectus muscles. He suggests that the increase in tonus can beexplained by the tendency of individuals with uncorrected

myopia to hold print or sewing excessively close to the eyes,with resulting development of esotropia.Our series of patients showed the following main char-

acteristics:

1. Esotropia had developed after the age of 16 years.2. The angle of deviation was similar for distance and

near fixation.3. Myopia was present in all but one patient.4. Esotropia and myopia were the only pathologic con-

ditions.5. Normal stereopsis was regained after surgical correc-

tion of the esotropia.

Table 1. Preoperative Data and Surgical Results of Patients with Acute Concomitant Esotropia of Adulthood

PatientNo.

Age(yrs)/

Sex

PreoperativeDeviation(Distanceand Near)

(PD)

Refraction(Spherical Equivalent)

Surgery

ImmediatePostoperative

Deviation(PD)

PostoperativeAdjustment

(PD)

Deviationon Last

Examination(PD)

Follow-upPeriod(yrs)RE LE

1 58/F ET 60 7.50 7.00 RE: MR Rec 7 mm AdjLR Res 10 mm

XT 25 3-mm advancementof MR

Orthophoria 4

2 18/M ET 20 3.75 5.25 RE: MR Rec 4 mm LE:MR Rec 5 mm Adj


E 4 3

3 36/F ET 25 7.00 7.75 RE: MR Rec 4 mm LE:MR Rec 4.5 mm Adj


E 6 4

4 31/M ET 55 6.0 6.0 LE: MR Rec 6 mm Adj;LR Res 10 mm


Orthophoria 5

5 54/F ET 45 1.5 2.0 LE: MR Rec 5.5 mm Adj;LR Res 7.5 mm


Orthophoria 4

6 21/F ET 25 2.75 1.0 RE: MR Rec 4.5 mm LE:MR Rec 5.0 mm Adj

Orthophoria None Orthophoria 3

7 22/M ET 18 1.5 1.5 LE: MR Rec 6.0 mm Adj E 8 0.5-mm recession ofMR

E 6 3

8 70/F ET 35 8.5 8.0 RE: MR Rec 6.0 mm AdjLE: MR Rec 5.5 mm

ET 12 1-mm recession ofMR

E 4 2

9* 24/M ET 25 3.5 4.5 RE: MR Re-Rec 2.0 mmAdj; LR Res 5.0 mm

Orthophoria None Orthophoria 2

10 49/F ET

30

2.0

2.0 RE: MR Rec 4.5 mm Orthophoria None Orthophoria 2LE: MR Rec 5.0 m Adj

Adj adjustable; ET esotropia; LE left eye; LR lateral rectus; MR medial rectus; PD prism diopters; RE right eye; Rec recession; Res resection; XT exotropia.*Second operation.

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These patients thus do not meet the criteria of the Swantype, because none of them had been subjected to occlusion ofone eye, and none had experienced loss of vision. Concomitantconvergent strabismus of the Franceschetti type is associatedwith a minimal amount of hypermetropia. Only one of thepatients met this criterion, but she had not experienced thephysical or psychic shock or exhaustion suggested to causeacute onset of the deviation in that type of esotropia.

Because all patients but one (90%) were myopic, theirtype of esotropia is closest to the concomitant convergentstrabismus originally described by Bielschowsky2 and latermodified by Hoyt and Good.4 Various degrees of myopia, aswell as constant and equal deviations at distance and at nearfixation, are consistent with this modified definition.

It is unclear why patients whose corrected visual acuityis normal in both eyes and who have normal stereopsis,develop strabismus at all. Bielschowskys explanation, im-plicating uncorrected myopia in the pathogenesis of theesotropia,2 can be eliminated as a factor in this series,because none of these patients had refrained from wearingtheir glasses for any significant length of time. Because all

of them regained normal stereopsis, decompensated mono-fixation syndrome could be excluded. Uncorrected hyper-metropia was also not an etiologic factor.

The absence of any pathologic signs other than the es-otropia and myopia suggests that serious pathology of thecentral nervous system is unlikely in these patients, al-though this assumption should be verified in larger studypopulations than that of this series. Such pathology is morelikely to be a factor if the esotropia is nonconcomitant.Nevertheless, concomitant esotropia does not preclude aserious neurologic condition, including a brain tumor.4

Therefore, the presence of an additional ocular or systemicsign (e.g., nystagmus) in these patients is sufficient to justifya neurologic and neuroradiologic investigation.3

Another acquired disorder of ocular horizontal versionthat results in esotropia is divergence insufficiency.5 Thissyndrome is characterized by ocular ductions and comitantesotropia only at distance, whereas at near fixation, thepatient is orthophoric. This type of strabismus differs fromthe type described in our series of patients, in whom devi-ation was the same for distance and near fixation.

The findings of this study are in agreement with those ofOhtsuki et al,6 who found no relationship between the timeof the operation and the postoperative development of ste-reopsis and no differences in the proportion of patients withbifixation between groups with early and delayed operation.All of the patients in this series achieved normal stereopsis

even though the operation was performed 2 to 5 years afterthe onset of esotropia.

In most of the published reports of late-onset or acute-onset esotropia, the study populations have included bothadults and children,69 and some have comprised childrenonly.1015 In the latter group of studies,1015 a large major-ity of the patients had hyperopic refraction. In the mixedseries of adults and children, however, whereas most of thechildren were hyperopic, most of the adults were myopic. Inone such study,8 in which 9 of the 10 patients were children,all of the children were hyperopic, and the single adult wasmyopic. Because our study population was restricted to

adults, it is proposed that the term acute concomitantesotropia of adulthoodbe used to describe this syndrome.The good binocular vision achieved after surgery by allof these patients can be explained as follows: binocularvision had apparently developed normally in all of thepatients before the onset of esotropia, and, therefore, itcould have been retained and later recovered after thestrabismus was corrected. Thus, whereas the term acute-

onset esotropia may be used to describe the syndrome inboth children and adults, it is suggested that the termacute concomitant esotropia of adulthoodbe restricted toolder patients only and that it be considered as one of thesubgroups of acute-onset esotropia. Other subgroups in-clude accommodative esotropia, acquired nonaccommo-dative esotropia of childhood, esotropia secondary toabnormalities of the central nervous system, esotropiasecondary to ocular sensory defects (this includes theSwan type), divergence paresis, and acute incomitantesotropia. Recent studies have shown that acquired non-accommodative esotropia of childhood is more prevalentthan congenital esotropia.16,17 In one of the studies per-

formed in these children,17

two with acquired nonaccom-modative esotropia developed bifoveal fixation after suc-cessful treatment, but most showed only some degree ofstereopsis (mean, 705 arc seconds).

By defining patients with acute concomitant esotropia ofadulthood as a separate subgroup, it is possible to charac-terize this subgroup in terms of certain common features,such as its association with myopia. Its most importantdistinguishing feature, however, relates to the surgicaloutcome. The success rate in re-establishing good stereo-scopic vision after surgery in this group of patients ishigh, unlike in children described as having esotropia ofacute onset.6,8,9

References

1. Burian HM, Miller JE. Comitant convergent strabismus withacute onset. Am J Ophthalmol 1958;45:55 64.

2. Bielschowsky A. Das Einwartsschielen der Myopen. DtschOphthalmol Gesell 1922;43:245 8.

3. Hoyt CS, Good WV. Acute onset concomitant esotropia: whenis it a sign of serious neurological disease? Br J Ophthalmol1995;79:498501.

4. Williams AS, Hoyt CS. Acute comitant esotropia in childrenwith brain tumors. Arch Ophthalmol 1989;107:376 8.

5. Wiggins RE Jr, Baumgartner S. Diagnosis and managementof divergence weakness in adults. Ophthalmology 1999;106:1353 6.

6. Ohtsuki H, Hasebe S, Kobashi R, et al. Critical period forrestoration of normal stereoacuity in acute-onset comitantesotropia. Am J Ophthalmol 1994;118:502 8.

7. Burian HM. Sudden onset of concomitant convergent strabis-mus. Am J Ophthalmol 1945;28:40710.

8. Legmann Simon A, Borchert M. Etiology and prognosis ofacute, late-onset esotropia. Ophthalmology 1997;104:134852.

9. Lyons CJ, Tiffin PA, Oystreck D. Acute acquired comitantesotropia: a prospective study. Eye 1999;13:61720.

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10. Lang J. Das Normosensorische essentielle konvergenteSpatschielen, eine Schielform sui generis. Klin MonatsblAugenheilkd 1978;172:80724.

11. Goldman HD, Nelson LB. Acute acquired comitant esotropia.Ann Ophthalmol 1985;17:777 8.

12. Watson AP, Fielder AR. Sudden-onset squint. Dev Med Child

Neurol 1987;29:20711.13. Clark AC, Nelson LB, Simon JW, et al. Acute acquired

comitant esotropia. Br J Ophthalmol 1989;73:636 8.

14. Ahmed S, Young JDH. Late onset esotropia in monozygous

twins. Br J Ophthalmol 1993;77:189 91.15. Dawson ELM, Marshman WE, Adams GGW. The role of

botulinum toxin A in acute-onset esotropia. Ophthalmology1999;106:172730.

16. Mohney BG. Common forms of childhood esotropia. Oph-thalmology 2001;108:8059.

17. Mohney BG. Acquired nonaccommodative esotropia in child-hood. J AAPOS 2001;5:859.

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