Alger, M.D.

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PARALYSIS OF DIVERGENCE.

*
ELLICE M. ALGER, M.D., New York.

If we are to judge from the number of cases reported in contemporary medical literature, paralysis of divergence, or indeed any of the so-called fusion paralyses, must be extremely uncommon. Since my attention was first directed toward the subject, nine cases have fallen under my observation. I feel pretty confident, however, that many cases pass unrecognized, partly because we have not had the condition in mind as a clinical entity, and partly because the definite diagnosis of ocular paralyses requires more time and better facilities than are usually available in clinical work. The movements of the eyes result,from impulses originating in or controlled by at least three different types of nervecenters. First, there are the motor centers, impulses from which are conveyed to individual muscles through the cranial nerves. Presiding over these are the cortical centers, through which we have the power of turning our eyes voluntarily in various directions. Finally, we have the so-called coordination or fusion centers, which, acting through the motor centers, automatically adjust the position of the eyes with regard to each other so that none of our voluntary movements shall result in double vision. Lesions involving the cranial nerves are common enough and are easily recognized. They cause a motor paralysis of the muscle or muscles of one eye supplied by the affected nerve. Lesions of the appropriate cortical areas, as in hemi* Candidate's thesis for membership accepted by the Committee on Theses. 665

ALGER: Paralysis of Divergence. plegia, result in inability to turn both eyes together to the right or left, or up or down, as the case may be, but they do not paralyze the muscles themselves, which are still capable of responding to stimulation from other sources, as in overcoming prisms. The so-called fusion paralyses are entirely different. We know that in certain individuals the fusion impulse is congenitally absent or latent; that in others it is very weak, while in still others it is capable of being suppressed or even destroyed, but as to its anatomic seat we have not the remotest idea. The fusion impulse may have a single localization, but the fusion performance is probably divided between several centers not necessarily very close together. For instance, we have occasionally cases in which the convergence power of the eyes seems to be entirely wanting, not because of any weakness of the muscles themselves, for the eyes can be rotated in various directions in a perfectly normal manner, but because the power of combining the action of the two interni in convergence has been lost. There seems to be a distinct center for convergence, for it may be lacking in patients whose other fusion powers are preserved. There seems to be also a divergence center coordinating the action of the two externi in the act of recovering from convergence or in overcoming prisms. It seems probable, too, that there are several other centers whose existence is so far merely a matter of hypothesis, awaiting the clinical proof of convincing illustrative cases. For instance, -a right hyperphoria, whether natural or caused by the action of a prism, results in a vertical diplopia, which is suppressed by the coordinated action of the right depressors and the left elevators. Indeed, there may be a' double center coordinating the action of the right inferior rectus and the left inferior oblique when the eyes are directed to the right, and the right superior oblique and the left superior rectus when they are directed to the left. A left hyperphoria is controlled by an
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entirely separate group of muscles, and may have a center or centers of its own, and the same may be argued of cyclophoria, the coordination of the inferior obliques in intorsion, and of the superior obliques in extorsion. Savage insists that there are at least twelve of these fusion centers. So far as I know there is no clinical confirmation of these centers by the definite paralysis of the co6rdination of muscles which are themselves not paralyzed at all, except in the case of convergence and divergence. The others may be much less common. They would certainly be much harder to prove conclusively beyond contravention. Divergence paralysis implies that a patient who can use either externus in a perfectly normal way in rotating his eyes voluntarily to the right or left has suddenly lost the power of combining their action in recovering from convergence. That keen clinical observer, Parinaud, reported the first case in 1883 ;2 the second case was also seen by him in 1889,3 but the whole subject was given new life by the scholarly paper of Duane,4 who pointed out the definite clinical symptoms which make it easy to recognize, and on the basis of which the symptoms of other fusion paralyses as yet unobserved can almost be foretold. Diagnosis.-As in all ocular paralyses in which the diagnosis is to be beyond dispute, the onset must be sudden. The chief subjective symptom is diplopia, which, from the resulting disturbances of orientation and projection, is frequently attended for a time by vertigo and nausea. The diplopia is a characteristic one. The divergence power being lost, the visual lines of the eyes tend toward each other, and according to Sherrington's law relaxation of one function, like divergence, automatically results in the stimulation of the opposite function of convergence. At any rate there is a convergent squint with homonymous diplopia when looking at distant objects. As the object of fixation is brought closer to the eyes, the images keep getting closer and closer to-

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gether until finally, at what Duane terms the "point of equilibrium," the visual lines cross and the double images are fused. If the object is carried still closer, the patient is able to maintain single vision by aid of his convergence power up to a point a few inches from the root of his nose. Within this point diplopia again occurs, because the limit of convergence power has been reached and this diplopia is "crossed." Duane has called attention to the fact that, when the object of fixation is approached to the eye till "single vision by approximation" is reached, the object can then be gradually withdrawn some little distance without diplopia recurring, and speaks of this as "single vision by recession." This was present in all my cases, and can perhaps be accounted for in this way: Paralyses of divergence automatically result in stimulation of convergence as the fixation point is approached to the eyes. When, however, it is carried away from them, convergence is automatically relaxed, and, though in this case it cannot be accompanied by any increase in the paralyzed function of divergence, the very relaxation permits some single vision by recession. When the patient looks straight ahead, neither externus receives any stimulation owing to the paralysis, but if the object be carried to either side, the externus on that side begins to receive its normal stimulation from the cortical centers for voluntary rotation which are not involved, and the diplopia perceptibly diminishes and in many cases even disappears entirely. This is, of course, quite different from the diplopia in motor paralysis, in which the rotation of the eyes in the direction of the weak muscle causes a tremendous increase in the amount of diplopia. Objective Symptoms.-When the patient looks at a distant object, he fixes it with the eye which has the best vision while its fellow turns in toward the nose, though not necessarily very markedly. If the fixing eye be covered, it turns it behind the screen, while the other can be seen to make an

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outward movement of redress, as it in turn takes up the task of fixation. As the screen is shifted from one eye to the other it can be seen that this deviation behind the screen is equal in the two, while in motor paralysis the difference is very perceptible. As the object is brought closer to the eyes both the deviation behind the screen and the movement of redress are seen to be smaller and smaller till the position of equilibrium is reached, when they cease entirely. Within this point the cover test shows a reversed (inward) movement of redress, at first hardly perceptible, but becoming very pronounced as the object is carried to the base of the nose. The voluntary movements of the eyes to the right or left in divergence paralysis should be perfectly normal. When roughly tested, the patient can move either cornea clear to the external canthus, and the more delicate tests of rotation with the perimeter or tropometer show no muscular weakness of either externus. Differential Diagnosis.-The conditions with which divergence paralysis is most likely to be confused, and their chief differences, are as follows: Conjugate Cortical Paralysis.-Both eyes may deviate to one side, but there is no apparent squint and no necessary diplopia. The patient cannot rotate both eyes together much beyond the midline in one or more directions, but convergence and divergence are preserved. Paralysis of one externus shows a greater diplopia, which increases tremendously as the fixation object is carried into the field of the paralyzed muscle and disappears entirely on the other side. The limitation of motion is marked by all tests, while the deviation under the cover test is much greater in the sound eye than in the diseased one, and increases as the object is carried to that side. Paralysis of both externi is characterized by much greater squint and wider diplopia. The diplopia increases instead of diminishes as the object of fixation is carried to either

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side, and there is inability to rotate either eye outward much beyond the midline. Convergence excess generally occurs in young subjects, and the condition is not a stable one, varying widely from day to day. Both diplopia and squint are much less marked for distant than for near tests, and are much increased if the accommodation is brought into play. Rough tests show no change in the rotation of the eyes, but careful measurements in all but the most recent cases show increased inward rotation and decreased outward. Divergence insufficiency is practically always the result of a previous convergence excess and has many of its symptoms. It is a fatigue condition, and is therefore neither sudden in its onset nor stable in its manifestation. The diplopia is less for distant objects and greater for near, and is very much increased by the use of the accommodation. It becomes less or disappears entirely after rest. Duane calls attention to the fact that the patient can maintain "single vision by recession" much further from the eyes than in paralysis of divergence. Causation.-In most of my cases there was the probability of an organic brain lesion of some sort. The first probably had a small cerebral hemorrhage. He had a chronic nephritis with very high tension, and during the preceding summer had an attack of unconsciousness lasting several hours. Case 2 showed marked evidences.of cerebral syphilis, while Case 3 was beyond doubt tabetic. Case 4 was diphtheritic, the first to be reported from this cause I think. Of Duane's personal cases, half were apparently due to organic brain disease, there being definite history of tabes, syphilis, multiple sclerosis, or brain tumor, while in the majority of the cases he collected from other sources the condition was so sudden and permanent as to justify the idea of a localized cerebral hemorrhage. Treatment.-In ordinary motor paralysis the patient soon

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learns to distinguish the true from the false image, and after a time learns either to suppress the latter entirely or to carry his head in such a position as to avoid the diplopia. At any rate, after a variable length of time all his subjective symptoms disappear, and it is often quite a task to make him conscious of his diplopia long enough for examination purposes. In divergence paralysis, however, the patient always has double images for distant objects which he can easily fuse at his reading distance, and it seems much more difficult for him to learn the psychic trick of suppression. Some of my patients either recovered entirely or learned it, but in others the diplopia persisted unchanged for years. In a number of Duane's cases the diplopia also persisted for long periods. It is, therefore, necessary to do something more than treat the cause of the condition. The most obvious resort seems to be the use of a prism base out before each eye. This plan of treatment is applicable only to cases where the diplopia is a moderate one, and such prLsms should, of couirse, be used only for distant vision, since their use for near would tend to provoke the very convergence excess which it is our particular wish to avoid, as in my seventh case. If they are necessary at all for near work, they should be made as w'eak as possible. Another point of importance is the correction of the hyperphoria, which seems to be present in a surprising proportion of the cases. Most latent squints result from refractive errors, and are kept under'control by the constant use of the fusion powers. It stands to reason then that, in divergence paralysis in which an important fusion element has been permanently destroyed, an unusually careful correction of the refraction should be made. It would seem that these cases, when of organic origin, were particularly suited for operative treatment after the laspe of a period of observation. The only operation that seems logical is the resection or advancement of both externi, attempting to secure even a divergence in such cases as have convergence

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excess. Such a procedure would carry the patient's point of equilibrium off to infinity, while by using his convergence power he would be able to maintain single vision up to points close enough for ordinary near work. CASE I. Mr. X, aged fifty-six years, referred by Dr. D. G. Sheehan, consulted me in November, 1909. For a week he had been having a severe attack of facial neuralgia which his physician had partially relieved with phenacetin. During the last two days the pain had practically ceased, but he had become conscious of a very annoying diplopia which he proceeded to describe. A man a block away on the street appeared to him like two men some distance apart, but as they approached him they kept getting closer together and at last merged into one. He had no diplopia for near objects, and had been able to read his paper without difficulty. He also noted the fact that, by turning his head in either direction, he could for a time at least suppress the diplopia for distance. He had been having a good deal of vertigo and nausea, which are so common in disturbances of the ocular equilibrium, but which he ascribed to his neuralgic attack. Examination of his eyes individually showed in each a moderately well-developed senile cataract. The fundus in each showed changes characteristic of arteriosclerosis: narrowing of arteries, indentation and tortuosity of veins, and one or two very small hemorrhages in each. His pupillary reactions were normal. His vision was somewhat reduced, being only 20/40 in each and not improved by glasses, though he was able to read fine type without much difficulty at the reading distance with his presbyopic correction. Examination of his binocular vision showed a homonymous diplopia by all tests of 160, the fixation light being 20 feet away. The diplopia was greatest in the primary position, diminishing and then disappearing entirely as he turned his head to the right or left. He had a right hyperphoria of 1.50, which did not change materially as he moved his eyes. As the test light was approached to him the diplopia became less and less and vision became single at ten inches. If the light was carried closer to the eyes than this, the screen

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test showed exophoria, while when the light was carried gradually further away he could maintain single vision some distance beyond the point where it occurred when the light was brought toward him. Measurement of the rotation of his eyes with the tropometer showed in the right an inward rotation of 500 and an outward one of 400, and in the left an inward of 550 and outward of 450, indicating a very moderate esophoria, but certainly no paralysis of either externus. These conditions were pretty constant during the week or ten days he was.under my observation. As an actor with serious professional responsibilities, he shortly went with his company on the road, and I never had an opportunity to examine his eyes again. He wrote me, however, many weeks later, that the diplopia had ceased to annoy him, and that under treatment of his physician he was in apparently very good health. He died suddenly of pneumonia while on tour. CASE II.-Seen in my clinical service at the Post-Graduate Hospital. Sarah G., a widow aged thirty-five years, born in Russia, had lost two children of diphtheria and her husband of tuberculosis. For two years she had had strabismus with diplopia, and had floated from one dispensary to another. Examination of her eyes showed media clear and fundi normal and vision 20/30 in each. Argyll-Robertson pupils. She had homonymous diplopia, securing single vision at 20 feet only by aid of a 250 prism base out. The diplopia diminished as she turned her eyes either to the right or to the left, and also when the light was brought closer to them, vision becoming single at a point four inches in front of her. If at this point the light was gradually withdrawn, she could maintain single vision up to 15 inches. Cover tests showed, when the fixation point was closer than four inches, a divergence, while at all points beyond this there was convergence of the visual axes. She had a right hyperphoria of 3. Her knee-jerks and other reflexes were greatly exaggerated, and though never able to get a Wassermann done, Dr. H. C. Cornwell was able to make a clinical diagnosis of cerebral syphilis before the patient disappeared from view. Neither was any exact measurement made of her powers of rotation, but clinically they appeared fully .up to the normal.
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CASE III was also seen in my service at the Post-Graduate Hospital. David S., aged forty-two years, had syphilis twenty years ago and had two years' treatment with inunctions and injections. Two years ago he began to have trouble in walking. Has lightning pains in various regions, an Argyll-Robertson pupil, static ataxia, and complete absence of patellar reflexes. A year ago he was suddenly conscious of double vision, with nausea and vertigo. An optician fitted him out with a pair of 40 prisms base out, and as he sees very much better with one eye t1an the other, the diplopia has not been very annoying. Examination of his eyes showed him to be myopic in each eye, but there were no abnormalities in either vision or fundi beyond those due to the myopia. He showed a homonymous diplopia of 120 by all tests, with a right hyperphoria of 10. The diplopia diminishes when the object of fixation is carried to the left or to the right, but does not disappear entirely. As a pencil is approached to him he sees it singly for the first time at a distance of 12 inches, and can maintain this single vision until it is withdrawn to 20 inches. Tipping his head forward lessens the diplopia. Objectively he shows a moderate convergent squint which diminishes under the cover test as the fixation point is brought nearer, until at a point of seven inches away the eyes are in a state of equilibrium. At a point four inches away the cover test shows an exophoria. Measurements of his rotatory power on a tropometer are rather below normal in all directions, but have a proper proportion and certainly show no evidence of any motor paralysis. CASE IV.-Mildred M., aged four years, first seen May 25, 1914. Two months ago the child had a mild attack of diphtheria and since that time swallows badly, regurgitates fluids through the nose, and talks with difficulty. A month ago she complained to her mother of seeing double. Examination of eyes shows media clear and fundi normal in both. Pupils react normally. Vision 20/40 each, increased to 20/20 by + 1 sph. Reads 20/20 and with sph. + 4 reads J. 1. Paralysis of accommodation. Diplopia of 200, homonymous, diminishing to 0 at six inches. Single vision by recession to 25 inches. Cover tests show the same

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measurements. Diplopia does not become either greater or perceptibly less when the fixation object is carried to right or left. There is no hyperphoria or vertical diplopia. The lateral rotations were normal. The child was never brought back for further examination, and I assume it went the same course as most diphtheritic paralyses. CASE V.-Miss E. C., aged sixty-two years, seen November 22, 1914. For the last five days has suffered from diplopia which came on suddqnly over night and is noted only for distant objects and does not interfere with reading. Patient has a low compound hyperopic astigmatism, but gets normal vision with either eye with correction and reads No.- 1 type. Pupillary reactions are normal. Media are clear, but both fundi show angiosclerosis, having notched, tortuous veins, and in the right eye a few small spots of exudate and in the left a small retinal hemorrhage. Homonymous diplopia of 200 at 20 feet, increasing very slightly eyes right, and diminishing but not disappearing eyes left. Also there is a perceptible left diplopia which does not increase eyes up or down. Single vision is obtained at six inches and maintained in recession to twelve. Even at this distance the diplopia tends to increase slightly when the fixation object is carried to the right, while it diminishes to the left. The rotations of the eyes to the right and left were not reduced in any way. I never saw this patient again, but her sister informed me afterward that the diplopia lasted for about two months and then disappeared (or was suppressed). CASE VI.-Mr. F. T., aged thirty-four years, patient of Dr. M. J. Echeverria, seen May 1, 1913. Doubtful history of specific infection several years ago, for which he has been thoroughly treated by several competent men, including a course at the Hot Springs. His Wassermann was negative a year ago. At that time his right eye began to turn in with the usual diplopia, and this has gradually increased, but for the last few months has remained stationary. Wears exclusion pad. Primary position shows a homonymous diplopia of 600 diminishing slightly, but distinctly both eyes right and eyes left. No hyperphoria. Single vision at two inches and by recession as far away as six inches. The

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squint does not increase in accommodation. Pupillary and other reflexes are normal. Tropometer measurements are 50 in and 40 outward in each eye. The media are clear and the fundi normal. He gets normal vision under atropin with sph. + 1.50 c cyl. + 0.37 ax. 90 in each eye. The motility is unchanged under cycloplegia. CASE VII.-Mr. L. H., aged thirty-seven years. Seen September 18, 1912. Has been in the army in the Philippines and had venereal warts, but gives no history indicative of syphilis. Wassermann not obtained. Is a chauffeur for a wealthy man, and seven months ago noticed that approaching cars were double and he was embarrassed in deciding which to dodge. Consulted a refracting optician who gave him a sph. - 0.75 with prism 20 base out in the right eye, and sph. + 0.75 with prism 50 base out in the left, which he has worn constantly. Sometimes he sees double with them at distance and he has constant headache. His media are clear and fundi normal. He has normal vision in each eye with sph. + 1 c cyl. + 0.50 ax. 90 in each eye, but vision is distinctly better with either eye alone than with both together. His pupillary reactions and reflexes are normal. He reads J. 1 with either eye. By all tests he shows a homonymous diplopia increasing slightly both to the right and the left. Diplopia diminishes as the fixation object is carried toward him, and disappears at six inches. Single vision by recession was noted but not measured. The ocular rotations were not reduced. I think in this case there was spasm of convergence resulting from wearing for. several months prisms base in which were too strong for anything except driving his car. I gave him full correction of his refraction and an exclusion pad. I learned from a relative a long time afterward that his headaches ceased promptly, and that finally he ceased to be troubled with diplopia; but he never came back for reexamination as advised, and it may have been merely suppressed. CASE VIII.-Mrs. A. N., aged fifty-four years, referred by Dr. W. J. Carpenter. Seen December 10, 1914. Patient has been a widow for thirty years with several healthy children, and has had no illness of any sort except that left breast was removed two years ago for a non-malignant

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neoplasm. Her urine is negative and her blood-pressure normal. Two months ago she began seeing double with some vertigo, but no headache or nausea. She has been myopic all her life, wearing sph. - 4.50 cyl. - 0.50 ax. 180 and reading without glasses. Examination showed media clear and fundi normal in both eyes, and her glasses were within a half diopter of her atropin correction, which gave her 20/20 in each. Pupils, accommodation and reflexes normal. By all tests she showed a homonymous diplopia of 90, diminishing slightly both eyes right and left. Also a right hyperphoria of 20 not increasing. Single vision by approximation at 18 inches, by recession to 48 inches. Ocular rotations as measured by tropometer 45 inward and 40 outward for both eyes. She was put on K. I. on general principles, and the diplopia gradually improved. When last seen, on March 26, 1916, it had the same characteristics, but single vision by approximation was secured at 4 feet and by recession up to 10 feet, while at times when she was not tired she claimed single vision.

CASE IX.-Mrs. J. W., aged sixty-five years, consulted me on January 15, 1916, with the following history: A year ago she first noticed a persistent diplopia when looking at distant objects, but not present close at hand, as in reading. She is not in very robust health, but her physician, after thorough examinations, says there is nothing organically wrong. Examination of her eyes revealed the following condition: Has beginning senile changes in both lenses, but otherwise both eyes show normal pupillary reactions, tension, and normal media and fundi. With sph. + 2 she gets normal vision with each, and with presbyopic correction reads J. 1. By all tests she shows a homonymous diplopia of 80, not increasing eyes right or left. Right hyperphoria 10, not increasing eyes up or down. Single vision by approximation at 18 inches and by recession as far as 48 inches. The rotations of both eyes in all directions were entirely normal.
1. 2. 3. 4.

REFERENCES. Barnes: Birmingham Med. Review, lxxxiii, 83, p. 232. Parinaud: Archiv. Neurol., March, 1883. Parinaud: Brain, iv, 1889. Duane: Ophthalmology, October, 1905.

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