Chapter 22: Anomalies of Convergence and Divergence

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Anomalies of Convergence and Divergence 501FIGURE 22–1. Active divergence elicited by prisms base-in. A, Electromyogram of right lateral rectusmuscle (upper tracing) and left lateral rectus muscle (lower tracing) before introduction of the prism.B, Increased activity of both lateral rectus muscles after 18 base-in was added while fusion wasmaintained. (From Tamler E, Jampolsky A: Is divergence active? An electromyographic study. Am JOphthalmol 63:452, 1967.)monkeys by means of electrical stimulation of the17, 44oculomotor area in the frontal lobe, whichsuggests the existence of a supranuclear controlmechanism for divergence. Second, the existenceof active convergence is universally accepted,even though Warwick 57 effectively shattered theFIGURE 22–2. Electromyogram during fusional divergencemovement. As the left eye of a patient with 17Dintermittent esotropia is uncovered (arrow), there is increasedactivity of both left and right lateral rectus muscles(LLR, RLR) as the eye makes a fusional divergenceeye movement. (From Tamler E, Jampolsky A: Is divergenceactive? An electromyographic study. Am J Ophthalmol63:452, 1967.)concept of Perlia’s nucleus acting as a convergencecenter. Thus the lack of more precise anatomicalinformation regarding the site of a divergencecenter does not dispose of the physiologicand clinical data that support an active divergencemechanism.Jampolsky, 30 although accepting the fact thatdivergence is an active mechanism, denied theexistence of nonretinal tonic vergence innervations.He rejected the concept of divergenceinsufficiency and paralysis and accepted only thefusional form of active divergence, that is, thatwhich is elicited by temporal disparity of retinalimages. It would exceed the purpose of this chapterto analyze this hypothesis, which is discussedfurther in Chapter 5, except to say that, in ouropinion, a tonic vergence mechanism has not beendisproved by the evidence presented. Moreover,one may argue that convergence and divergenceparalyses, as well as convergence nystagmus, arewell-recognized entities that cannot be explainedsolely on the basis of deficient fusional divergence,14 that accommodation is not necessarilydefective in convergence insufficiency, and thatexperimentally administered ethanol 6, 15, 45 and barbiturates58 have been shown to affect the tonic
502 Clinical Characteristics of Neuromuscular Anomalies of the Eyevergence mechanism. Furthermore, Scott 50 reportedelectromyographic findings in a patientwith V exotropia that could not have been causedby anything but tonic divergence.Anomalies of ConvergenceConvergence InsufficiencyETIOLOGY AND CLINICAL FINDINGS. Convergenceinsufficiency is one of the most commoncauses of ocular discomfort and, in fact, is themost common cause of muscular asthenopia;therefore it is of considerable clinical significance.There is frequently an etiologic connectionwith associated accommodative difficulties. Forinstance, a convergence insufficiency as a resultof disuse of the accommodative convergencemechanism may have been caused by uncorrectedhigh hypermetropia or myopia. Patients with hypermetropiaexceeding, say, 5D or 6D, make littleor no effort to accommodate, and in those withmyopia there is no need to accommodate to obtainclear vision at near fixation. Likewise, a patientwith beginning presbyopia may develop convergenceinsufficiency after wearing a bifocal prescriptionfor the first time. The relief of sustainedaccommodative effort afforded by the new prescriptioncauses a decrease of accommodativeconvergence; thus an exophoria that had been controlledby accommodative convergence may becomemanifest. In other patients without refractiveproblems the condition may arise without anyobvious cause.Some ophthalmologists consider patients withconvergence insufficiency to be neurotic and believethat their problem is something to be dealtwith by a psychiatrist. We emphatically reject thisgeneralization. 11 The often dramatic subjective improvementafter appropriate therapy, noted concurrentlywith the objective clinical finding of improvednear point of convergence and fusionalconvergence amplitudes, clearly puts this conditionon an innervational basis.In rare instances acquired convergence insufficiencymay occur on an organic basis, such assecondary to a subdural hematoma. 52An admirably concise description of the symptomsarising from convergence insufficiency wasgiven by von Graefe, who pointed out as early as1855 26, 27 that such patients complain about eyestrainand a sensation of tension in and about theglobes. After brief periods of reading, the letterswill blur and run together; crossed diplopia occasionallyoccurs during near work. Characteristically,one eye will be closed or covered whilereading to obtain relief from visual fatigue. Littlecan be added to this classic description except thatocular headaches are another frequent complaint.Von Graefe thought that convergence insufficiencywas myogenic, that is, caused by a congenitalweakness of the medial rectus muscles secondaryto overaction of the lateral rectus muscle. He recommendedprisms base-out to exercise the actionof the medial rectus muscles in some patients,prisms base-in to eliminate symptoms in others,or a weakening procedure of the lateral rectusmuscles. Except for prisms base-out, which arestill used by some, his views on the etiology ofconvergence insufficiency and therapeutic suggestionshave not withstood the test of time.DIAGNOSIS. The diagnosis of convergence insufficiencyis based on the finding of a remote nearpoint of convergence and decreased fusional convergenceat near fixation. The reader is referred toChapter 12 for a discussion of diagnostic methodsand the clinically important differentiation betweenthe subjective and objective near point ofconvergence. Most patients with convergence insufficiencyexhibit varying degrees of exophoriaat near fixation; however, this disorder also occursin patients with orthophoria and occasionally evenin those with esophoria. The near point of accommodationis normal and corresponds to the age ofthe patient. However, to identify patients who sufferfrom a combined insufficiency of convergenceand accommodation (see p. 503) and who requirea different form of therapy, the near point ofaccommodation should be determined in eachcase. 41Convergence insufficiency seldom becomes aclinical problem until a patient reaches the teenageyears. Increased schoolwork and prolonged periodsof reading may then exacerbate the characteristicsymptoms. The type of patient most oftenencountered is a high-school, college, or universitystudent who is especially prone to developsymptoms before examinations when special demandsare made on the near vision complex duringextended periods of studying. Needless to say,symptoms are aggravated by lack of sleep, reductionof general well-being, and anxiety.THERAPY. Therapy for convergence insufficiencyis in the realm of orthoptics. Indeed its treatment
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Chapter 22: Anomalies of Convergence and Divergence

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