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Knapp LectureWhy do the eyes cross? A review and discussion othe nature and origin of essential infantile esotropmicrostrabismus, accommodative esotropia, andacute comitant esotropiaEmilio C. Campos, MDa,b

PURPOSE To try to explain the long-term stability of bilateral medial rectus botulinum toxin ( botox)chemo-denervation in essential infantile esotropia; to evaluate divergent fusion amplitudein accommodative esotropia and acute comitant esotropia of emmetropes; to look foraccommodation anomalies in high AC/A ratio accommodative esotropia and acute comi-tant esotropia of myopes; and to discuss characteristics of microstrabismus.

METHODS Retrospective analysis of 61 essential infantile esotropia patients with early treatment with onebotox injection in both medial rectus; measurement of divergent fusion amplitude in accom-modative esotropia and acute comitant esotropia; measurement of Near point of accommo-dation in high AC/A ratio accommodative esotropia and acute comitant esotropia of myopes.

RESULTS Stable results were found in 85.24% of essential infantile esotropia treated patients; reduceddivergent fusion amplitude was detected in accommodative esotropia and acute comitantesotropia; hypo-accommodation was found in some patients with high AC/A ratio accommo-dative esotropia and a convergence spasm in acute comitant esotropia of myopes.

CONCLUSIONS Very early botox treatment probably eradicates the effect of an excessive convergencetonus in essential infantile esotropia. A prevention of accommodative esotropia with fullretinoscopic correction is only mandatory with a significantly reduced amplitude offusional divergence. A deficit in accommodation should be looked for in high AC/A ratioaccommodative esotropia, before bifocal lenses prescription. Early diagnosed acute co-mitant esotropia of myopic patients can be treated as a convergence spasm. Only surgerytreats acute comitant esotropia, in patients with emmetropia or moderate hypermetropia.

( J AAPOS 2008;12:326-331)

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problem does not pertain to paralytic or mechanicbismus, where the lesion is self-explanatory. Costrabismus is still a big mystery. I shall try to addrissue and discuss those elements requiring furthercation, dealing separately with essential infantile eso

Author affiliations: aProfessor of Ophthalmology, University of Bologna, bChieOphthalmology, St. Orsola-Malpighi Teaching Hospital, Bologna, Italy

Presented at the 34th Annual Meeting of the American Association for PedOphthalmology and Strabismus Washington DC, April 2-6, 2008.

This study was supported in part by MIUR (ex 60%) and in part by a graFondazione Cassa di Risparmio in Bologna.

Submitted February 28, 2008.Revision accepted March 24, 2008.Published online June 12, 2008.Reprint requests: Prof. Emilio C. Campos, U.O. di Oftalmologia, Unive

Policlinico St. Orsola-Malpighi, via Palagi, 9, 40138 Bologna, Italy (emaiemilio.campos@unibo.it).

Copyright © 2008 by the American Association for Pediatric OphthalmologStrabismus.

1091-8531/2008/$35.00 � 0doi:10.1016/j.jaapos.2008.03.013

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microstrabismus, accommodative esotropia, and acmitant esotropia.

Essential Infantile EsotropiaThe term essential infantile esotropia, which includesgenerally labeled congenital esotropia, was introdu1984 by a group of strabismologists (the InternStrabismus Study Group) and voiced by von Noornumerous occasions.1 Several attempts have beenduring the last century to establish its etiology. Apahistorical theories, such as those put forward by Wand Chavasse,3 defects in the sensory mechanismbinocular cortical cells have been put forward as a cstrabismus.4-6 Yet excellent sensory binocular coophas been detected in 4-month-old infants who evebecame esotropic.7,8 Moreover, it has never been dstrated that defects in the binocular cortical cellpresent before esotropia. Finally, binocular sensoryalies, that is, suppression and anomalous retinal corrdence, can be eliminated with treatment and cannot

fore be considered as cause of strabismus.

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Volume 12 Number 4 / August 2008 Campos 327

A defect in the motor fusion mechanism hathought to be the factor responsible for esotropia fothan 2 decades.9 If both eyes are not used propegether at an age when the binocular visual systemits plasticity, the normal disparity detection mechthat is, motor fusion, deteriorates. Anomalous disinduced vergence movements have been shown to dparticularly in early-onset esotropia.10-13 The purpthese movements is to maintain a stable angle of devThus they can be a hindrance to positive surgical reAttempts have been made to overcome this proboptical means ( prisms),14-16 surgery17 and, more rethrough chemodenervation of the medial rectus mwith the use of botulinum toxin A.18 It is not clear wthe aforementioned phenomena represent the expof an excessive convergence tonus (esotonus) orreinforcement of anomalous vergence movemenesotonus.

Indeed, Jampolsky19,20 has repeatedly pointed oactive convergence as an active binocular functionbe differentiated from esotonus as an innervationthat is centrally driven by unequal visual input toeyes. Convergence is a mechanism for which thdeviate from a baseline, under normal conditionssory input. When sensory input conditions are altereyes return to baseline because of tonus. BrodsFrey21 point out that monocular esotonus is a cainfantile esotropia, whereas convergence is an effecther, they relate infantile esotropia to dissociatedtion.22 These theoretical considerations are extremteresting and potentially promising for our understof the etiology of infantile esotropia. It remainsestablished what triggers the prevalence of esotosome patients only—those who develop essential inesotropia even with equal visual input to the 2 eyethe role of potential differences between saccadesferent directions.23

A brief review of our results of injection of bottoxin A into both medial rectus muscles for essenfantile esotropia may be of some interest.24 Botoriginally injected in one rectus muscle of humancreating an incomitant strabismus, and injectionoften repeated.25-27 We started to inject both medtus muscles simultaneously in very young patientsage, 6.5 months) in 1989 and published our first re1992.18 We never injected our patients more thanOur candidates for botulinum toxin treatment had tstrict requirements24; for this reason, our seriestively limited (61 treated patients). One high-dosetion of botulinum toxin (at least 3 units for each minduced large-angle exotropia in all patients. Onbotulinum toxin wore off, this large-angle exotrocame orthotropia or more often small-angle esotropviation not larger than 10�).

Our follow-up time is now quite long. Stablecould be obtained in 85.24% of treated patients. I

61 patients, the botulinum toxin injection in the medi

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rectus muscles even eliminated elevation in adductidissociated vertical deviation, which were orpresent. In recent years, greater doses (up to 4 unitnecessary, as the botulinum toxin now available appbe less effective than it once was. Our results havreplicated by others,28-32 who even reported therence of stereopsis in some patients after treatmIndeed, a single injection of botulinum toxin hastemporary effect on muscle function. Evidently, assequence of artificial exotropia, the system redresseIt remains to be explained whether this takes place bvergence movements or esotonus have been weaModulation of neurotoxins’ effect is difficult. Mygrowth factors have been very recently shown to dmuscle strength in animals and appear to be a prosubstitute for neurotoxins.33

In essence, if the 2 eyes lose their perfect coesotonus takes over, and an esotropia develops.3

almost-magnetic push toward adduction can probabbe interrupted at very early ages with the creatiotemporary exotropia. It remains to be demonstratmost infants do not overadduct. In other wordskeeps the eyes straight? Are the benefits of normalular vision sufficiently relevant to justify the urge teyes straight?

Strictly related to this problem is a further questipertains to the stability of the effect of surgery in einfantile esotropia in the absence of motor imbalanof amblyopia of one eye. Why does the system asurgically induced variation of the angle of strabeven if the procedure is performed relatively late? Wfound significantly longer refixation times in freelynating patients with large-angle as compared withwith small-angle strabismus. Prolonged refixationalso are found for the nonfixing eye of patients whoalternate fixation. This could explain why freely aling patients try to maintain a small-angle deviatiocould infer that patients control the deviation betrapid alternation of fixation is possible. Distance ption is also better in small-angle versus large-angbismus.37 Conclusive answers are not available. Cea better modulation of the final outcome of surgeryfeasible once the disturbing elements are identifiethis reason, all existing computer-assisted models fobismus surgical indications are effective only in incostrabismus.38-42 Changes in programming of theence copy” (internal copy of a motor innervation) coconsidered. The possibility that muscle propriocmay also play a role cannot be excluded, althoueffects of changes in eye muscle proprioceptiextremely limited in size and tend to wear ofrapidly.43-47

Finally, the origin of motor sequelae of essentialtile esotropia remains puzzling, despite the numeroories which have been proposed. These includenystagmus, elevation in adduction, and dissociated

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Volume 12 Number 4 / August 2008328 Campos

MicrostrabismusVarious names have been used for a primary strathat is strictly nonalternating and of such a reducedto be immeasurable.53 Microtropia, microstrabismmonofixational syndrome essentially coincide.54-5

original suggestion that microstrabismus can coexinormal binocular vision55 cannot be corroboratefollowing elements are always present: inconspicuogle of deviation (smaller than that one detectablecover test), anomalous retinal correspondence, gabsent stereopsis, and amblyopia in the nonfieye.57-60 Anisometropia is often present, but thepatients with equal refraction. Hence, anisometrose cannot be considered the etiological factor for mtrabismus. No proof exists to support the hypothepreexisting binocular sensory anomalies are the cmicrostrabismus.54 Moreover, even disparity detecnormal in the periphery, but absent or pathologicacenter.60 For the aforementioned reasons, micromus may be considered as part of a spectrum thfrom normal binocularity and orthophoria to strawithout normal binocular vision.57 Intermediate staheterophoria, fixation disparity, and microstrabismessence, the 2 eyes cannot be kept “in register” fromand the visual cortex is incapable of correcting thistive cooperation. Therefore, as in large-angle strabanomalous correspondence in microstrabismus maadaptation to an oculomotor anomaly that occurscentral vision, because there are other mechanismunknown—that render the visual system insensilarge disparities associated with nonfixated objects.viously, this condition is not preventable, and a consamblyopia can only be diagnosed early, but not pre

Accommodative EsotropiaSince the work of Donders,62 we know that uncohypermetropia can cause esotropia. An accommeffort induces excessive convergence, hence the dement of esotropia. This is proved by the fact thatfull correction of the hyperopic refractive error pnormal binocular vision. Yet, 3 problems should bsidered. First, not all hypermetropic patients deveotropia. Second, in some patients, full hyperopiction eliminates the deviation for distance but not foThird, asthenopic complaints are found in sevetients at a certain age despite of the use of full hypcorrection.

Recommendations have been made for preventieral risk factors for accommodative esotropia fromoping.63,64 Fusional amplitude in divergence hasbeen considered. To assess its role, we selected 30 pages 5 to 9 years with hypermetropia ranging from5.50 D. Fifteen were orthophoric without glasses,were esotropic without glasses but orthophoric witfull retinoscopic correction. In the first group, div

fusion amplitude, as measured with prisms, was betwee

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8� and 10� for distance and between 10� and 14� ffixation. In the second group, it ranged between 2�

for distance and between 4� and 8� for near fiTherefore, a significant difference between the 2existed. Obviously, we have no elements to excluthe use of the full retinoscopic correction wouldthe divergent fusional amplitude but, rationally, tpears to be unlikely. From a practical point of viepossible to infer that a full retinoscopic correction idatory in all hypermetropic children with a limitedgent fusion amplitude.

The second issue pertains to excessive convergenear fixation despite full retinoscopic correctioncondition has been defined as nonrefractive accomtive esotropia57 and is usually dealt with initiallbifocal lenses. After several years, if a deviationpresent for near fixation, a bilateral medial rectus reis performed, usually with excellent results. An accodative deficit, that is, an early (or innate) presbyopbe found after a patient’s prolonged use of bifopointed out by von Noorden and Jenkins.65 It haargued that this deficit could be attributed to the puse of bifocals. Yet in 10 of 28 consecutive patiwhom bifocals were prescribed by us at age 5 to 8the near point of accommodation (NPA)—measurethe Prince ruler and recorded in diopters—waslower range of normal, that is, approximately 10 D,1 of bifocal lenses prescription, thus suggestive of hcommodation. The number of subjects in this gextremely limited, but our preliminary resultsthat parents should be warned— before bifocaprescribed—that their children may continue to renear add in their teenage years. It can be concludedleast in some patients, convergence excess is attributhypoaccomodative esotropia, as described by Cbader66 and subsequently confirmed by others.67,68

A final aspect to consider is asthenopic complainmay be detected at approximately 12-14 years ofaccommodative esotropia patients. These complaiattributable to esophoria, present despite the totalopic correction. This superimposed esophoriarequires surgical attention and may be caused bygressive weakening of divergent motor fusion omodification of refraction. Only the phoric comshould be surgically addressed. Bilateral medial reccessions are effective even if, theoretically, bilateralrectus resections are an option.

Acute Comitant EsotropiaThis condition can be found both in myopia andmetropia/low hypermetropia. Von Graefe69 first deesotropia in myopes, whereas it was Bielschowskyeventually analyzed this condition in depth. Burianlater Franceschetti72 identified acute esotropia of p

n with emmetropia/low hypermetropia.

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Volume 12 Number 4 / August 2008 Campos 329

Acute comitant esotropia is characterized by theonset of diplopia at distance. Binocular single visnear is initially retained. In the literature, this condoften confused with decompensation of esophoriadiplopia starts at near) and esotropia caused by neuical conditions such as Arnold-Chiari malformWhereas surgery can be performed immediately afdiagnosis in myopic patients, there should be a delaleast 6 months in emmetropic patients, in whomimaging is required, as there may be an associatiointracranial lesions. In the case of Arnold-Chari mmation, esotropia can be eliminated by neurosdecompression.73

The origin of acute comitant esotropia is uncbilateral deficit of the abducens nerve and/or a diveparalysis74 have been postulated as causative eleMore recently, acute comitant esotropia has beenered as a sort of horizontal skew deviation, in somrelated to cerebellar lesions.52

We evaluated 21 myopic patients with comitantpia (aged 25 to 35 years) and 14 emmetropic patienesotropia (aged 21 to 32 years). In myopic patientsgent fusional amplitudes were within normal limitsing from 9� to 12� for distance and from 10� to 1near. In emmetropic patients, divergent fusionaltudes were reduced, ranging from 4� to 6� for distanfrom 8� to 10� for near.

Bielschowsky’s acute comitant esotropia is characby a tendency for relapses, which may occur a few mor several years after surgery. This type of straappears as an endless tendency toward convergentherefore speculated that Bielschowsky’s acute coesotropia might be attributable to a spasm in convedue to a change in the myopic prescription. An incrlens power or even a modification of the frame canan increase in induced hypermetropia for near, domby an excess of accommodation and therefore of cgence. The latter cannot be relaxed for distanceand diplopia develops. To eliminate the convespasm we prescribed atropine and bifocals in 5 cBielschowsky’s esotropia. The condition resolved ipatients after 2 to 5 months, and surgery was notsary; however, follow-up is not available for these pbeyond 2 years. Larger series and longer follow-unecessary to substantiate this finding. From a ppoint of view, great care must be used before incremyopic prescription.

On the other hand, Burian-Franceschetti’s acutetant esotropia shows reduced divergence fusion ampIt responds well to bilateral medial rectus recessiorelapses are generally not encountered. Lang75 descnormo-sensorial late-onset esotropia in childrencondition was rediscovered more than 10 years lateroften related to a history of psychosocial problemtients suddenly develop strabismus and experiencepia. Immediate surgery is indicated and has excellen

tional results. We also obtained favorable results wit

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botulinum toxin chemodenervation of both medialmuscles.18 These data were recently confirmed bers.77 There is no reason to doubt that this formbismus is different from the Burian-Franceschettiobserved in adults.

In conclusion, in this lecture I have tried to shayou my thoughts and my experience on severalwhich deserve further attention. I hope to haveraised your interest in areas that certainly deservin-depth investigation.

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