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Etiology of Heterophoria and Heterotropia

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Etiology of Heterophoria and Heterotropia CHAPTER 9 Etiology of Heterophoria and Heterotropia n heterophoria there is a relative deviation of Factors Responsible for the Ithe visual axes held in check by the fusion Manifestation of a Deviation mechanism, whereas in heterotropia there is a manifest deviation of the visual axes. The relative Abnormalities of Fusion Mechanism position of the visual axes is determined by the equilibrium or disequilibrium of forces that keep DEFECT OF MOTOR FUSION IN INFANTILE ES- the eyes properly aligned and of forces that disrupt OTROPIA. Motor fusion in patients with hetero- this alignment. Clearly, the fusion mechanism and phoria is adequate to maintain a proper alignment its anomalies are involved in some manner in of the eyes. This does not mean that patients with producing comitant heterotropias. To understand a heterophoria necessarily have normal sensory the etiology of neuromuscular anomalies of the fusion. In those with higher degrees of heteropho- eyes, therefore, one should also gain an insight ria, suppression and a high stereoscopic threshold into other factors that determine the relative posi- may be present, but motor responses are sufficient tion of the visual axes. to keep the eyes aligned. In heterotropia this is First, there are anatomical factors, which con- not the case. These circumstances have led to a sist of orientation, size, and shape of the orbits; theory of the etiology of strabismus developed by size and shape of the globes; volume and viscosity Worth in 1903 in his famous book on squint.156 of the retrobulbar tissue; functioning of the eye His theory was that the essential cause of squint muscles as determined by their insertion, length, is a defect of the fusion faculty156, p. 55 and indeed elasticity, and structure; and anatomical arrange- is a congenital total absence of the fusion fac- ment and condition of fasciae, ligaments, and pul- ulty.156, p. 61 Worth did not make a distinction be- leys of the orbit. tween sensory and motor fusion. Second, there are innervational factors, that is, Worth’s theory has had an enormous influence all the nervous impulses that reach the eyes. These on the thinking about strabismus, especially about factors include the co-movements of extraocular essential infantile esotropia, but objections to it muscles with intrinsic ocular muscles, psycho- have been raised. In fact, Chavasse,24 in editing optical reflexes (fixation reflex, fusional impulses), the seventh edition of Worth’s Squint, went so far influences of the static apparatus on extraocular as to say muscles and their tonus (endolymph, vestibular We need no longer vainly genuflect before the fireless system, reflexes from neck muscles), and influ- altar of ‘‘defect of the fusion faculty’’; anymore than ences of the several nuclear and supranuclear areas we need be content to regard lameness (with which that govern ocular motility. strabismus has so much in common) as a defect of the 134 Etiology of Heterophoria and Heterotropia 135 walking faculty [p. 2] . To many it will be a relief Modern psychophysical research in infants5, 134 to see the exposure . of ‘‘congenital defect of fusion has made it possible to add to the rather ancient faculty’’ as a superstition which may have had its uses in the past [p. viii]. theory of Worth. It has become evident that motor and sensory components of binocular vision such The comparison with lameness limps, as do most as visual acuity,66 contrast sensitivity,8, 11 stereop- comparisons. Lameness may result from many sis,7, 68 and retinal disparity sensitivity causes, among them a defect in the ‘‘walking (vergences)67 are incompletely developed at birth faculty,’’ that is, incoordination of the impulses to (see also Chapter 11). The infantile visual system muscle, as in tabetic ataxia, or from paralysis of a appears especially vulnerable to destabilization muscle with contracture of the antagonist. In most during this state of visual immaturity. The absence instances, however, lameness has little in common of a strong vergence control mechanism in the with comitant strabismus. presence of a weak sensory input may explain the To assess what Worth meant, one must reread high prevalence of transient esotropias or exotro- what he wrote. He stated that when the fusion pias in infants that later develop normal binocular faculty is inadequate ‘‘the eyes are in a state of vision.54, 109 With maturation of motor fusion, sta- unstable equilibrium, ready to squint either in- bilization of ocular alignment occurs. However, if 156, p. 55 wards or outwards on slight provocation.’’ development of motor fusion is delayed or if mo- Precipitating factors may be hypermetropia, aniso- tor fusion (i.e., the vergence system) is primarily metropia, motor anomalies, specific fevers, violent defective, perhaps from genetically determined mental disturbances, injury during birth, occlu- factors, esotropia may develop under the influence sion, and hereditary factors. In other words, Worth of a variety of strabismogenic causes.110 These makes no claims other than that the factors that may include excessive tonic convergence, hyper- lead to a latent deviation become manifest in the metropia, anisometropia, anomalies of the neural absence of a proper fusion mechanism. By general integrator for vergence movements, and other fac- agreement, this is how heterophoria and hetero- tors still unknown. Held,67 who proposed a similar tropia are defined. working hypothesis for the etiology of essential One must admit that Worth’s proof for his infantile esotropia (see also Helveston69), points concept of a congenital weakness of the fusion out that this theory, while speculative, has the faculty156, p. 61 is not conclusive. He cited the exam- ple of a young patient with alternating esotropia advantage of being testable with available meth- and normal vision in each eye, no refractive error, ods. Further reference to this theory is made in and no detectable motor anomalies. Hypermetro- Chapter 16. pia and mechanical elements therefore are ex- SENSORY OBSTACLES TO FUSION. Observa- cluded as etiologic factors. When tested with the tions in older patients leave no doubt that interfer- amblyoscope, the patient suppressed the image ence with fusion may precipitate a manifest devia- from one eye and no amount of exercise enabled tion in predisposed patients. The interference may him to fuse the two images. The esotropia, Worth be of peripheral or central origin and produce reasoned, must be the result of a congenital total sensory or motor obstacles to fusion. Among the absence of the fusion faculty when, in fact, this peripheral sensory obstacles are conditions that patient’s inability to fuse probably resulted from a materially reduce the vision in one eye or the well-established suppression mechanism rather patching of either eye. A result of patching is well than from a primary fusion defect. Indeed, consid- illustrated by the following example. ering that Worth, as stated above, did not make a distinction between sensory and motor fusion, one could conceive here that the original problem was CASE 9–1. in the motor fusion mechanism and that suppres- sion took place as a consequence of the loss of A 14-year-old boy had a large chalazion of the right ocular alignment. Another finding difficult to rec- lower lid. After removal of the chalazion, he wore a oncile with a primary sensory fusion defect is bandage over the eye for 2 days. When the bandage the observation that some patients with essential was taken off he complained of diplopia. He now infantile esotropia show a remarkably high degree had an alternating esotropia of 40⌬. The visual acuity ם of sensorimotor binocular cooperation (subnormal was 6/6 in each eye and a hypermetropia of 5.0 110 sphere D was present OU. He was given the refrac- binocular vision) after surgical alignment of the tive correction which he had never worn before and eyes (see Chapter 16). 136 Introduction to Neuromuscular Anomalies of the Eyes fit-over base-out prisms that restored single binocu- the patient of the diplopia. Two years later she had lar vision. The strength of the prisms was reduced an esophoria of 2⌬ for distance and 8⌬ of exophoria every 2 or 3 days. After 2 weeks the manifest devia- for near, with correction. Binocular cooperation was tion had entirely disappeared, but an esophoria re- normal. mained for distance of about 20⌬, with correction. Both with and without correction, the boy had excel- lent fusional amplitudes and full stereopsis. The pa- Cases 9–2 and 9–3 are examples of transient tient refused to wear his refractive correction. Since his vision was excellent, he had no symptoms and or permanent impairment of the fusion mechanism the glasses were in his way. Throughout 2 years of from traumatic or toxic causes. Toxic causes also observation the condition remained unchanged. It may be the precipitating factors in heterotropias should be added that the boy’s older brother had of childhood, although it is difficult to prove this been operated on for esotropia. point. In a significant number of cases it can be established only by the history. Parents are known to be prone to attribute an ocular deviation in their In essence, Case 9–1 demonstrates that a pe- children to an incidental cause—a fall or disease. ripheral sensory obstacle, in this instance brief Yet, knowing how severe the toxic effect of dis- occlusion of one eye, is capable of precipitating a eases such as measles or whooping cough may be large manifest deviation when ordinarily a well- on the central nervous system, it is not unreason- functioning fusion mechanism would prevent such able to formulate the hypothesis that these condi- an anomaly. A similar problem may also be caused tions may precipitate heterotropia in some chil- by centrally acting factors, as shown by the fol- dren.
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