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Diplopia of Provocation*
DIPLOPIA OF PROVOCATION 6. Orthoptic training may be beneficial following surgery in cases of this type. Medical Arts Building (1).
87
I wish to thank Dr. R. H. Millwee for his kind ness in supplying the X-ray films reproduced in Figures 4 and 5.
REFERENCES
1. Brown, A., and Harper, R. K.; Craniofacial dysostosis: The significance of ocular hypertelorism. Quart. J. Med., (New Series), 15 :171-182 (July) 1946. 2. Balding, G., Surgery for paralysis of the external rectus muscle. Eye, Ear, Nose & Throat Monthly, 26:144-146 (Mar.) 1947. 3. Scobee, R. G.: The Oculorotary Muscles. St. Louis, Mosby, 1947, p. 346. 4. Walker, J. P. S.: Brit. J. Ophth., 19:477-479 (Sept.) 1945. 5. Payne, B. F.: Am. J. Ophth., 26:390-393,1944. 6. Hummelsheim, E.: Arch. f. Augenh., 62:71,1908.
DIPLOPIA OF ITS
PROVOCATION*
NEUROLOGIC S I G N I F I C A N C E
J E A N S E D A N , M.D.,
AND S I M O N E S E D A N - B A U B Y ,
M.D.
Marseille, France Translator: F. HERBERT HAESSLEH, M.D., Milwaukee, Wisconsin W e present a description of a new neuro logic test, which we have termed "diplopia of provocation," and some brief comments on its mechanism, its varieties, its clinical use, and its future possibilities. It was originally conceived in order to study the latent motor deficiencies which remain after the total clini cal disappearance of ocular paralyses. Soon, however, we discovered that its possibilities were more extensive. Thus, it is now pos sible for us to suggest that diplopia of provo cation has a definite place in the clinical neuro-ophthalmic tests. I. U N D E R L Y I N G P R I N C I P L E S
In a patient in whom an ocular muscle appears to be normal after a more or less prolonged paralysis, a prism of 20 to 45 degrees is placed in front of the eye that was paralyzed (both eyes being open) in such a position as again to produce, as exactly as possible, the initial spontaneous pathologic paralysis. Conditions must be such that the ♦First presented before the Societe d'Ophthalmologie de Paris, June 21, 1947.
formerly paralyzed muscle is not stimulated to contract. T o select the degree of prism we use the lucite prism bar of Dr. Conrad Berens. T h e patient must, and this is extremely un pleasant, endure, with both eyes open, the diplopia brought on by the prism for at least 15 to 30 minutes and sometimes even up to 120 minutes. T h e test is without value unless there is no neutralization of the prism and unless the diplopia exists without intermis sion during its entire course. It is at the end of the test, which we call "prismatization," when the prism is taken away, that the diplopia of provocation is pro duced. Fusion is restored immediately in normal subjects, but a residual diplopia per sists in certain old ophthalmoplegias. W e are dealing here with a true "diplopia of reap pearance" which follows the application of the test prism and survives its removal. W i t h our colleague, Claude Boudon of Vichy, we made our first observations on a patient who still had convergence asthenopia after temporary ophthalmoplegia of the
JEAN SfiDAN AND SIMONE SfiDAN-BAUBY
88
fourth cranial nerve. As this patient pro gressed toward complete cure, the duration of the periods of diplopia of provocation lessened and it was possible to follow the gradual straightening-out process. In so far as we have been able to discover, there is not a single reference to this sub ject in the literature. Only Comberg (Klin. Monatsbl. f. Augenh., 3:120, 1945) seems to have approached the phenomenon which we have described. His work, however, does not deal with reinvoking a diplopia that has disappeared clinically. On the contrary, through the use of prisms, he reveals the presence of a pathologic condition progress ing toward diplopia. II.
AIMS
Our test belongs essentially in the general class of tests of provocation and has as its purpose: (1) The study of latent motor deficiences following ophthalmoplegias; (2) a more minute study than is at present possible of the exophorias and convergence insufficiencies; (3) the definition, by the crossing and uncrossing of the diplopia of provocation, of the trend toward aggrava tion or improvement of latent ophthalmo plegias; (4) the exploration of various im portant neurologic syndromes of ocular symptomatology which have not been mani fest but in which our test of provocation will be able to show heretofore unsuspected ocu lomotor damage. In fact, by means of the diplopia of provo cation, it should be possible to measure not only the state of the muscle studied, but also the general cause of its injury, whether it was due to syphilis, diabetes, or even to cere bral tumor. Serial examinations indeed per mit a true "measured" tabulation of the cause of the paralysis and its degree. We have been able to establish by clinical observation, that, in the phenomenon we are describing, a true muscular deficiency has re appeared and that it is not a compensatory hypercontraction of the antagonist. Experi
mentally, by atropinization for example, it is possible to show that accommodation main tains convergence and has absolutely no ef fect on provoked diplopia. III.
METHOD
Diplopia of provocation manifests itself only when it has been able to reproduce the initial paralysis exactly and for a fairly long period. Nor does it occur under condi tions in which the formerly paralyzed muscle has been put into play. The choice of the best position to give to the prism to elicit most easily the diplopia of provocation is a point of exceptional in terest. The first thought is to place the prism in such a way that the formerly para lyzed muscle must contract to avoid the di plopia created by the provoking prism. If the muscle does not succeed in this, there remains, after this useless and powerful ef fort, a deficiency which is also exploited by the antagonist and whose expression is itself the diplopia of provocation. This is what some have called the "logical position" of the prism of provocation. It is by placing the prism in the "illogi cal" position, that is, in the opposite direc tion, that we observe the clearest and most lasting diplopias of provocation. Everything occurs, then, as if the recently paralyzed muscle, placed in absolute inaction by the prism during the provocation, regains its contractility only slowly and with difficulty, when the removal of the prism again gives full and complete freedom to the oculomotor antagonists which then carry on without dif ficulty. Unfortunately, we are not yet suffi ciently rich in experiments to draw formal conclusions on this subject. IV. DURATION
The duration of the diplopia of provoca tion depends on the duration of the applica tion of the test prism, the degree of original paralysis, the time of its clinical disappear ance, the degree of progress toward a cure of
89
DIPLOPIA OF PROVOCATION its cause, the exact type of the paralysis (homonymous diplopias reappear more easily by provocation than those connected with injury of the adductors), and on the general condition of the subject (for example, mere fatigue or actual illness). The usual duration of secondary diplopias is about 30 minutes, but we have noted dura tions of 2, 6, 48, and, once, even of 90 hours. No rule governing the respective durations of prism-induced diplopia and secondary prism-free diplopia can be formulated, but we can affirm that in no case have any un pleasant after-effects been observed. Never theless, it takes much persuasion to induce the patient, who is naturally disturbed by the reappearance of his trouble, to submit to the test. V. MEASUREMENT AND VARIETIES
We deal generally with a microdiplopia of not more than one degree. The angle of de viation must be measured with the Maddox cross which is more precise than the perim eter. The latter brings on a troublesome dis comfort by the proximity of its arc. One can obtain an approximate measurement with the Maddox rod or with colored glasses. Practice has taught us that certain di plopias of provocation do not occur except after a specific excitation, perhaps as a result of a long duration of prismatization, or be cause of the extreme power of the prism, or finally because of the necessary repetition of prismatization. An important complication that often thwarts our efforts and makes the interpreta tion of our results more difficult is the ha bitation to the test prism which appears in the course of experiments among the old ophthalmoplegics who are perfectly stabi lized. To conquer this habituation it becomes necessary to increase the strength of the prism, or to lengthen or repeat the sessions of prismatization. Two varieties of diplopia of provocation
would seem to be most worthy of attention at the present time. The first, which may prove to be of considerable importance to neurolo gists, is the induced diplopia, so named be cause the prismatization provokes persistence of double vision after removal of the pro vocative prism in certain subjects who are neurologically deficient but ocularly intact even though these subjects had never before known double images. The second, which we call diplopia of se lection, permits analysis on a physiologic plane of the various elements of a complex ophthalmoplegia. The least-affected pair of cranial nerves ceases, after a time, to pro voke diplopia by its disuse and only the di plopia connected with the most-affected oculomotor nerve persists. For example: A young woman, apparently cured of an ophthalmoplegia specifically in volving the sixth nerve and a part of the third (right superior), reacted by a consider able and confused diplopia of provocation to prismatization of 30 minutes. A quarter of an hour after removal of the prism, the hori zontal doubling (sixth pair) disappeared and only the vertical (third pair) diplopia re mained. We thus learned that the greatest in jury was to the third nerve. Although the diplopia of selection is the most recent pos sibility our test has disclosed, we are certain there are other possibilities not, as yet, de tected or identified. VI.
OBSERVATIONS
By means of the provocative prism test, it has been possible to reevoke the latent se quelae of paralysis in patients who were ap parently cured. This has been done in cases of: paralysis of the oblique that resulted from palpebral focal infection; paralysis of the external oculomotor of diabetic origin; common oculomotor paralysis of traumatic origin; injury of the sympathetic, occurring in the course of treating a frontal mucocele; paralysis of the external ocular muscle after freezing; involvement of the external
90
JEAN SfiDAN AND SIMONE SfiDAN-BAUBY
oculomotor in facial paralysis following grippe; paralysis of the common oculomotor in three tertiary syphilitics; paralysis of the external oculomotor of glaucomatous origin; paralysis of the common oculomotor after cerebral hemorrhage and after relapse of cerebral tumors. Nothing is more impressive in an old pa tient operated for cerebral tumor, with an ophthalmoplegic episode recorded previous to intervention and cured by it, than to see the duration of diplopia of provocation grad ually diminish for an identical period of prismatiziation. In this way it is possible to ob tain a true measure of the extent of the orig inal pathologic process and the degree of progress toward cure. CONCLUSIONS
We would like to acquaint American oph thalmologists and neurologists with the test of diplopia of provocation because we be lieve that the test is capable of giving a true measure of the lesion and of its cause. The fact that, with the diplopia of provo
cation, one can follow an absolutely silent lesion in the course of routine clinical in vestigation, give a controllable prognosis at any time, watch the success or failure of a therapy, and, finally, can extend the explora tion to affections still without evident oculo motor symptoms makes it seem worth while to us to make our work known and to ad vocate its general use. We certainly do not belittle the infinite patience that the application of our test takes on the part of the observer, the good will and absolute confidence that it exacts from the subject observed, the infinite disappoint ments that this research involves, and the fact that the interpretation of its results is not always immediately accessible. But the fact that the test will confirm or correct a neuro-ophthalmologic diagnosis makes it seem worthy of the attention of clinicians of whom we ask only that they study it with an open mind and, through experimentation much greater than our own, to give it practical and general evaluation. 94 Rue Sylvabelle.
REFERENCES
Sedan, J., and Sedan-Bauby, S.: Diplopie de provocation. Bull. Soc. d'opht. de Paris, June 21, 1947; Bull, de la Ste. d'opht. de Paris, Oct., 1947, pp. 321-328. : Premiers resultats de l'etude des diplopies de provocation en neuro-clinique oculaire. Rev. Oto-neuro-ophtal., 19:257-277 (July) 1947. : Sur quelques varietes de la diplopie de provocation. Ste. d'oto-neuro-ophtal., November 29, 1947. •: Presentation de deux schemas sur les mecanismes possibles de la diplopie de provocation. Ste. oto-neuro-ophtal. du Sud-Est, November 29, 1947. : Les diplopies de provocation; leur signification neurologique. Presse med., Jan. 10, 1948, p. 22. : Diplopie de creation, diplopie de selection. Congres Soc. frang. d'opht. Paris, May, 1948. —: La diplopie de provocation nouveau test de neuro-syphilimetrie. Marseille-med., 1948.
87
I wish to thank Dr. R. H. Millwee for his kind ness in supplying the X-ray films reproduced in Figures 4 and 5.
REFERENCES
1. Brown, A., and Harper, R. K.; Craniofacial dysostosis: The significance of ocular hypertelorism. Quart. J. Med., (New Series), 15 :171-182 (July) 1946. 2. Balding, G., Surgery for paralysis of the external rectus muscle. Eye, Ear, Nose & Throat Monthly, 26:144-146 (Mar.) 1947. 3. Scobee, R. G.: The Oculorotary Muscles. St. Louis, Mosby, 1947, p. 346. 4. Walker, J. P. S.: Brit. J. Ophth., 19:477-479 (Sept.) 1945. 5. Payne, B. F.: Am. J. Ophth., 26:390-393,1944. 6. Hummelsheim, E.: Arch. f. Augenh., 62:71,1908.
DIPLOPIA OF ITS
PROVOCATION*
NEUROLOGIC S I G N I F I C A N C E
J E A N S E D A N , M.D.,
AND S I M O N E S E D A N - B A U B Y ,
M.D.
Marseille, France Translator: F. HERBERT HAESSLEH, M.D., Milwaukee, Wisconsin W e present a description of a new neuro logic test, which we have termed "diplopia of provocation," and some brief comments on its mechanism, its varieties, its clinical use, and its future possibilities. It was originally conceived in order to study the latent motor deficiencies which remain after the total clini cal disappearance of ocular paralyses. Soon, however, we discovered that its possibilities were more extensive. Thus, it is now pos sible for us to suggest that diplopia of provo cation has a definite place in the clinical neuro-ophthalmic tests. I. U N D E R L Y I N G P R I N C I P L E S
In a patient in whom an ocular muscle appears to be normal after a more or less prolonged paralysis, a prism of 20 to 45 degrees is placed in front of the eye that was paralyzed (both eyes being open) in such a position as again to produce, as exactly as possible, the initial spontaneous pathologic paralysis. Conditions must be such that the ♦First presented before the Societe d'Ophthalmologie de Paris, June 21, 1947.
formerly paralyzed muscle is not stimulated to contract. T o select the degree of prism we use the lucite prism bar of Dr. Conrad Berens. T h e patient must, and this is extremely un pleasant, endure, with both eyes open, the diplopia brought on by the prism for at least 15 to 30 minutes and sometimes even up to 120 minutes. T h e test is without value unless there is no neutralization of the prism and unless the diplopia exists without intermis sion during its entire course. It is at the end of the test, which we call "prismatization," when the prism is taken away, that the diplopia of provocation is pro duced. Fusion is restored immediately in normal subjects, but a residual diplopia per sists in certain old ophthalmoplegias. W e are dealing here with a true "diplopia of reap pearance" which follows the application of the test prism and survives its removal. W i t h our colleague, Claude Boudon of Vichy, we made our first observations on a patient who still had convergence asthenopia after temporary ophthalmoplegia of the
JEAN SfiDAN AND SIMONE SfiDAN-BAUBY
88
fourth cranial nerve. As this patient pro gressed toward complete cure, the duration of the periods of diplopia of provocation lessened and it was possible to follow the gradual straightening-out process. In so far as we have been able to discover, there is not a single reference to this sub ject in the literature. Only Comberg (Klin. Monatsbl. f. Augenh., 3:120, 1945) seems to have approached the phenomenon which we have described. His work, however, does not deal with reinvoking a diplopia that has disappeared clinically. On the contrary, through the use of prisms, he reveals the presence of a pathologic condition progress ing toward diplopia. II.
AIMS
Our test belongs essentially in the general class of tests of provocation and has as its purpose: (1) The study of latent motor deficiences following ophthalmoplegias; (2) a more minute study than is at present possible of the exophorias and convergence insufficiencies; (3) the definition, by the crossing and uncrossing of the diplopia of provocation, of the trend toward aggrava tion or improvement of latent ophthalmo plegias; (4) the exploration of various im portant neurologic syndromes of ocular symptomatology which have not been mani fest but in which our test of provocation will be able to show heretofore unsuspected ocu lomotor damage. In fact, by means of the diplopia of provo cation, it should be possible to measure not only the state of the muscle studied, but also the general cause of its injury, whether it was due to syphilis, diabetes, or even to cere bral tumor. Serial examinations indeed per mit a true "measured" tabulation of the cause of the paralysis and its degree. We have been able to establish by clinical observation, that, in the phenomenon we are describing, a true muscular deficiency has re appeared and that it is not a compensatory hypercontraction of the antagonist. Experi
mentally, by atropinization for example, it is possible to show that accommodation main tains convergence and has absolutely no ef fect on provoked diplopia. III.
METHOD
Diplopia of provocation manifests itself only when it has been able to reproduce the initial paralysis exactly and for a fairly long period. Nor does it occur under condi tions in which the formerly paralyzed muscle has been put into play. The choice of the best position to give to the prism to elicit most easily the diplopia of provocation is a point of exceptional in terest. The first thought is to place the prism in such a way that the formerly para lyzed muscle must contract to avoid the di plopia created by the provoking prism. If the muscle does not succeed in this, there remains, after this useless and powerful ef fort, a deficiency which is also exploited by the antagonist and whose expression is itself the diplopia of provocation. This is what some have called the "logical position" of the prism of provocation. It is by placing the prism in the "illogi cal" position, that is, in the opposite direc tion, that we observe the clearest and most lasting diplopias of provocation. Everything occurs, then, as if the recently paralyzed muscle, placed in absolute inaction by the prism during the provocation, regains its contractility only slowly and with difficulty, when the removal of the prism again gives full and complete freedom to the oculomotor antagonists which then carry on without dif ficulty. Unfortunately, we are not yet suffi ciently rich in experiments to draw formal conclusions on this subject. IV. DURATION
The duration of the diplopia of provoca tion depends on the duration of the applica tion of the test prism, the degree of original paralysis, the time of its clinical disappear ance, the degree of progress toward a cure of
89
DIPLOPIA OF PROVOCATION its cause, the exact type of the paralysis (homonymous diplopias reappear more easily by provocation than those connected with injury of the adductors), and on the general condition of the subject (for example, mere fatigue or actual illness). The usual duration of secondary diplopias is about 30 minutes, but we have noted dura tions of 2, 6, 48, and, once, even of 90 hours. No rule governing the respective durations of prism-induced diplopia and secondary prism-free diplopia can be formulated, but we can affirm that in no case have any un pleasant after-effects been observed. Never theless, it takes much persuasion to induce the patient, who is naturally disturbed by the reappearance of his trouble, to submit to the test. V. MEASUREMENT AND VARIETIES
We deal generally with a microdiplopia of not more than one degree. The angle of de viation must be measured with the Maddox cross which is more precise than the perim eter. The latter brings on a troublesome dis comfort by the proximity of its arc. One can obtain an approximate measurement with the Maddox rod or with colored glasses. Practice has taught us that certain di plopias of provocation do not occur except after a specific excitation, perhaps as a result of a long duration of prismatization, or be cause of the extreme power of the prism, or finally because of the necessary repetition of prismatization. An important complication that often thwarts our efforts and makes the interpreta tion of our results more difficult is the ha bitation to the test prism which appears in the course of experiments among the old ophthalmoplegics who are perfectly stabi lized. To conquer this habituation it becomes necessary to increase the strength of the prism, or to lengthen or repeat the sessions of prismatization. Two varieties of diplopia of provocation
would seem to be most worthy of attention at the present time. The first, which may prove to be of considerable importance to neurolo gists, is the induced diplopia, so named be cause the prismatization provokes persistence of double vision after removal of the pro vocative prism in certain subjects who are neurologically deficient but ocularly intact even though these subjects had never before known double images. The second, which we call diplopia of se lection, permits analysis on a physiologic plane of the various elements of a complex ophthalmoplegia. The least-affected pair of cranial nerves ceases, after a time, to pro voke diplopia by its disuse and only the di plopia connected with the most-affected oculomotor nerve persists. For example: A young woman, apparently cured of an ophthalmoplegia specifically in volving the sixth nerve and a part of the third (right superior), reacted by a consider able and confused diplopia of provocation to prismatization of 30 minutes. A quarter of an hour after removal of the prism, the hori zontal doubling (sixth pair) disappeared and only the vertical (third pair) diplopia re mained. We thus learned that the greatest in jury was to the third nerve. Although the diplopia of selection is the most recent pos sibility our test has disclosed, we are certain there are other possibilities not, as yet, de tected or identified. VI.
OBSERVATIONS
By means of the provocative prism test, it has been possible to reevoke the latent se quelae of paralysis in patients who were ap parently cured. This has been done in cases of: paralysis of the oblique that resulted from palpebral focal infection; paralysis of the external oculomotor of diabetic origin; common oculomotor paralysis of traumatic origin; injury of the sympathetic, occurring in the course of treating a frontal mucocele; paralysis of the external ocular muscle after freezing; involvement of the external
90
JEAN SfiDAN AND SIMONE SfiDAN-BAUBY
oculomotor in facial paralysis following grippe; paralysis of the common oculomotor in three tertiary syphilitics; paralysis of the external oculomotor of glaucomatous origin; paralysis of the common oculomotor after cerebral hemorrhage and after relapse of cerebral tumors. Nothing is more impressive in an old pa tient operated for cerebral tumor, with an ophthalmoplegic episode recorded previous to intervention and cured by it, than to see the duration of diplopia of provocation grad ually diminish for an identical period of prismatiziation. In this way it is possible to ob tain a true measure of the extent of the orig inal pathologic process and the degree of progress toward cure. CONCLUSIONS
We would like to acquaint American oph thalmologists and neurologists with the test of diplopia of provocation because we be lieve that the test is capable of giving a true measure of the lesion and of its cause. The fact that, with the diplopia of provo
cation, one can follow an absolutely silent lesion in the course of routine clinical in vestigation, give a controllable prognosis at any time, watch the success or failure of a therapy, and, finally, can extend the explora tion to affections still without evident oculo motor symptoms makes it seem worth while to us to make our work known and to ad vocate its general use. We certainly do not belittle the infinite patience that the application of our test takes on the part of the observer, the good will and absolute confidence that it exacts from the subject observed, the infinite disappoint ments that this research involves, and the fact that the interpretation of its results is not always immediately accessible. But the fact that the test will confirm or correct a neuro-ophthalmologic diagnosis makes it seem worthy of the attention of clinicians of whom we ask only that they study it with an open mind and, through experimentation much greater than our own, to give it practical and general evaluation. 94 Rue Sylvabelle.
REFERENCES
Sedan, J., and Sedan-Bauby, S.: Diplopie de provocation. Bull. Soc. d'opht. de Paris, June 21, 1947; Bull, de la Ste. d'opht. de Paris, Oct., 1947, pp. 321-328. : Premiers resultats de l'etude des diplopies de provocation en neuro-clinique oculaire. Rev. Oto-neuro-ophtal., 19:257-277 (July) 1947. : Sur quelques varietes de la diplopie de provocation. Ste. d'oto-neuro-ophtal., November 29, 1947. •: Presentation de deux schemas sur les mecanismes possibles de la diplopie de provocation. Ste. oto-neuro-ophtal. du Sud-Est, November 29, 1947. : Les diplopies de provocation; leur signification neurologique. Presse med., Jan. 10, 1948, p. 22. : Diplopie de creation, diplopie de selection. Congres Soc. frang. d'opht. Paris, May, 1948. —: La diplopie de provocation nouveau test de neuro-syphilimetrie. Marseille-med., 1948.