Chapter 22: Anomalies of Convergence and Divergence

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Anomalies of Convergence and Divergence 505rotic persons. Such patients will exhibit intermittentepisodes of sustained maximal convergenceassociated with accommodative spasm (inducedmyopia) and miosis. The functional nature of thiscondition is emphasized by the finding that suchpatients may have tubular field defects. In someinstances, the spasm can be triggered by askingthe patient to fixate an object held closely beforethe eyes. After the fixation object has been removed,the eyes will remain in a convergent position,as demonstrated by Case 22–1.CASE 22–1A 28-year-old female school teacher complained ofintermittent double vision and blurring. Her visualacuity was 6/6 OU without correction. Refractionrevealed emmetropia. Examination of ocular motilityshowed orthophoria at distance. During the coverand the cover-uncover test at near fixation, the patient’seyes suddenly converged, she complained ofdiplopia, and her pupils had become miotic. Shemaintained convergence after removal of the fixationtarget. Refraction was repeated, and myopia of6D was now present in each eye. After 12 minutesthe eyes returned spontaneously to a normal position.On further questioning the patient complainedabout a multitude of bizarre symptoms. She wasreferred to a psychiatrist who diagnosed ‘‘hysteria.’’Souders 51 reported convergence spasm in twoneurotic persons. The clinician should be aware,however, that convergence spasm may have anorganic basis, and it has been reported to occurafter encephalitis, tabes, labyrinthine fistulas, 5trauma, 20; 56, p.239 Arnold-Chiari malformation, pituitaryadenoma, and posterior fossa neurofibroma. 19Thus patients with spasm of the near reflex shouldundergo neurologic evaluation to exclude theseorganic causes. 19 Bielschowsky 3 reported convergencespasm with traumatic unilateral depressorparalysis in a patient in whom a spasm of convergenceand accommodation occurred after an attemptto overcome the vertical diplopia.Unless an organic cause can be found, therapyconsists of prolonged atropinization of the eyesand plus lenses prescribed as lower segment bifocals.Monocular occlusion may also be considered.This treatment may have to be applied for manymonths, sometimes for as long as a year, beforethe convergence spasm subsides and the patientregains visual comfort.Anomalies of DivergenceDivergence InsufficiencyDivergence insufficiency is regarded as a separateand benign clinical entity to be differentiated fromdivergence paralysis and bilateral cranial nerveVI paresis. It is characterized by intermittent orconstant esotropia at distance fixation with symptomaticuncrossed diplopia in patients who maintainfusion at near. Characteristically, the angle ofstrabismus is the same in primary position andlateral gaze. Fusional divergence is reduced markedlyboth at distance and near fixation. Unlike inthe case of divergence paralysis, the neurologicfindings are normal.The literature contains relatively few reportsdealing with divergence insufficiency. 12, 29, 38, 42, 46 Adistinction between divergence insufficiency andparalysis is by no means an easy task in everycase, nor is it always possible. On clinicalgrounds, however, whenever possible we find ituseful to differentiate between a patient with esotropiaof sudden onset at distance fixation in theabsence of neurologic disease (divergence insufficiency)and one in whom this event is associatedwith a history of head trauma, hypertensive vasculardisease, or other neurologic problems (divergenceparalysis). In divergence insufficiency withoutneurologic signs we first use prisms base-outin the amount required to give the patient comfortablesingle vision at distance fixation. This prescriptionusually does not interfere with singlebinocular vision at near fixation but if it does,upper segment Fresnel prisms are prescribed.Since divergence insufficiency is a self-limitingcondition, the prisms usually can be reduced inpower after several weeks or months and eventuallybe dispensed with. However, if the patientdoes not respond to prisms, resection of both lateralrectus muscles should be considered 11, 36 andadjustable sutures are advisable. 35Divergence ParalysisDivergence paralysis was described first as a clinicalentity by Parinaud, 43 who observed patientswith a sudden onset of homonymous diplopia atdistance fixation in whom ductions and versionswere normal. Many subsequent cases have beenreported. 10, 21, 24, 32 Among the underlying diseasesmost frequently cited to be etiologically significantare tabes, encephalitis, disseminating sclerosis,
506 Clinical Characteristics of Neuromuscular Anomalies of the Eyepseudotumor cerebri, 30 poliomyelitis, 23; 56, p.238 influenza,2 vascular lesions involving the vertebrobasilararterial system, 18 neoplasms, 9, 34, 36 increasedintracranial pressure, and head13, 31, 54trauma, 33 in which divergence paralysis may beassociated with papilledema. 48 Even though theexistence of divergence paralysis has been disputedfor a long time, many current authors haveaccepted it. 29 Bielschowsky 4 discussed the difficultiesencountered in making the diagnosis ofdivergence paralysis and pointed out how frequentlythis condition may be simulated by paresisof one or both lateral rectus muscles. He observedseveral cases of lateral rectus paresis in whichcomitance developed rapidly, and within a matterof a few weeks the motility defect became indistinguishablefrom divergence paralysis. Jampolsky30 expressed the view that divergence paralysisdoes not exist and that all such patients actuallyhave a bilateral cranial nerve VI paresis. Kirkhamand coworkers 31 reported three patients with increasedintracranial pressure and divergence paralysis.The deviation remained unchanged inlateroversion, but the electro-oculographically determinedsaccadic velocities were significantly reducedin abduction, which attests to weakness oflateral rectus muscle action. After the patientsrecovered, symptoms of divergence paralysis subsidedand saccadic velocities in abduction returnedto normal. These authors concluded that cranialnerve VI pareses, caused by increased intracranialpressure, may produce symptoms of divergenceparalysis without other evidence of cranial nerveVI palsy and without the need to evoke a specificlesion involving the divergence mechanism.Hence a clear distinction between divergencepalsy and lateral rectus muscle paresis may bedifficult at times, or even impossible, since onecondition may merge with the other.On the other hand, the evidence from carefullyconducted studies of individual cases is sufficientlyconvincing to consider divergence paralysisas a clinical entity separate from a bilateralcranial nerve VI paresis. Several findings clearlyinculpate the divergence mechanism and cannotbe explained on the basis of bilateral abducensnerve paresis: (1) fusional divergence is markedlyreduced or absent if measured from the fusionfreeposition at near and distance fixation, (2) theesotropia not only remains unchanged but mayeven decrease in lateroversion, 14, 21, 43 and (3) saccadicvelocities are only mildly reduced, as arecent study of 12 patients with the clinical findingsof divergence paralysis has shown. 35According to Bielschowsky, 4 the diagnosis ofdivergence insufficiency or paralysis is based onthe following criteria: (1) there is a sudden onsetof uncrossed diplopia at distance fixation, (2) theangle of strabismus remains unchanged or maydecrease on lateroversion, (3) when an object isbrought nearer to the patient, the two images approacheach other and are finally fused when theobject is at a distance of 25 to 40 cm from thepatient, and (4) the field of fixation is unrestricted.Bielschowsky 4 also pointed out that divergenceparalysis occasionally may be confused with convergencespasm. In both instances the patient willcomplain of uncrossed diplopia at distance fixation;however, in convergence spasm, fusional divergenceis unimpaired and visual acuity at distanceis decreased.REFERENCES1. Adler FH: Pathologic physiology of strabismus. Arch Ophthalmol50:19, 1953.2. Anselmi P: Contributo clinico alla paralisi della divergenza.Riv Otoneurooftalmol 39:659, 1964.3. Bielschowsky A: Symptomatologie der Störungen imAugenbewegungsapparat. In Bunke O, Foerster O, eds:Handbuch der Neurologie, vol 4. Berlin, Springer-Verlag,1936, p 173 ff.4. Bielschowsky A: Lecture on Motor Anomalies. Hanover,NH, Dartmouth College Publications, 1943/1956, p 152 ff.5. Borries GVT: Konvergenzspasmus und Labyrinthleiden.Monatsschr Ohrenheilkd 60:736, 1926; cited in ZentralblGes Ophthalmol 17:912, 1927.6. Brecher GA, Hartman AP, Leonard DD: Effect of alcoholon binocular vision. Am J Ophthalmol 39:44, 1955.7. Breinin GM: The nature of vergence revealed by electromyography.III. Accommodative and fusional vergence.Arch Ophthalmol 58:623, 1957.8. Brown HW: Strabismus in the adult. In Haik GM, ed:Strabismus. Symposium of the New Orleans Academy ofOphthalmology. St Louis, Mosby–Year Book, 1962, p 259.9. Brown S, Iacuone JJ: Intact sensory fusion in a child withdivergence paresis caused by a pontine glioma. Am JOphthalmol 128:528, 1999.10. Bruce GM: Ocular divergence: Its physiology and pathology.Arch Ophthalmol 13:639, 1935.11. Burian HM: Anomalies of the convergence and divergencefunctions and their treatment. In Symposium on Strabismus.Transactions of the New Orleans Academy of Ophthalmology.St Louis, Mosby–Year Book, 1971, p 223.12. Burian HM, Brown AW: Unusual adverse effect of prismaticcorrections in a child with divergence insufficiency.Am J Ophthalmol 74:336, 1972.13. Chamlin M, Davidoff L: Divergence paralysis with increasedintracranial pressures (further observations). ArchOphthalmol 46:195, 1951.14. Cogan DG: Convergence nystagmus with notes on a singlecase of divergence nystagmus. Arch Ophthalmol 62:295,1959.15. Colson ZW: The effect of alcohol on vision. An experimentalinvestigation. JAMA 115:1525, 1940.16. Costenbader FD: The physiology and management of di-
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Chapter 22: Anomalies of Convergence and Divergence

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