|Year : 1959 | Volume
| Issue : 1 | Page : 1-36
Aetiology of synkinetic oculo-palpebral movements in congenital and acquired ophthalmoplegias
Department of Ophthalmology, Irwin Hospital, Delhi, India
|Date of Web Publication||7-May-2008|
N S Jain
Department of Ophthalmology, Irwin Hospital, Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Jain N S. Aetiology of synkinetic oculo-palpebral movements in congenital and acquired ophthalmoplegias. Indian J Ophthalmol 1959;7:1-36
|How to cite this URL:|
Jain N S. Aetiology of synkinetic oculo-palpebral movements in congenital and acquired ophthalmoplegias. Indian J Ophthalmol [serial online] 1959 [cited 2020 Oct 20];7:1-36. Available from: https://www.ijo.in/text.asp?1959/7/1/1/40703
Foremost, it is my pleasant duty to thank the All-India Ophthalmological Society for giving me this opportunity of delivering the Adenwalla Oration for the year 1950. The honour is mine but the credit for this research is shared. I owe my extreme indebtedness for cooperation to all the members of the staff of the Department of Ophthalmology of Irwin Hospital, Delhi, particularly Dr. D. V. Sethi, Dr. R. C. Agarwal and Dr. Om Prakash. For help in photography I wish to thank Mr. Kalyan Singh. For allowing me to reproduce some illustrations from my paper already published (Jain, 1957-a) my thanks are due to the Editorial Committee of the British Journal of Ophthalmology.
My interest in the subject of abnormal lid movements associated with the anomalies of ocular movements was aroused when I came across nine cases in quick succession between the months of July and October, 1956. These were subsequently reported in the British Journal of Ophthalmology (Jain, 1957-a). Thereafter, as I studied at a great length a large number of cases of congenital and acquired ptosis and/or ophthalmoplegias, I felt that many of the aetiological theories suggested by several authors in the past were not supported by experimental and surgical proofs to elucidate some neurophysiological facts and so required a more critical study. Observing 100 cases my conclusions are presented in this paper.
| Clinical Material|| |
The material for study, classified as under, is presented in three parts for the purpose of discussion :-
I. Congenital cases (29 cases) - No.Of Cases
A. Those which did not show synkinetic movements ….. 25
B. Those which showed synkinetic movements of the same side ….. 1
C. Those which showed widening and Retraction Syndrome ….. 3
II Acquired Cases. Associatd with involvement of III,VI and sympathetic nerves (32 cases)
A. Those which did not show synkinetic movements …. 14
B. Those which showed retraction, phenomena on side to side and downward gaze …. 11
C. Inconclusive, therefore not described …. 7
III. Exophthalmometric observations .. … …. 39
| Congenital Cases|| |
A. Those Which did not Show Elevation of the Lid
Of the twenty-five consecutive cases of congenital ptosis seen, none showed a lid retraction of the ptosed lid on occlusion of the sound eye.
Out of these, 19 were unilateral and 6 were bilateral.
Unilateral cases : The function of the superior rectus was normal in all. Both the eyes maintained a parallelism of the visual axes in all directions of the gaze, all ocular movements being normal. With a normal function of the superior rectus and not showing a lid retraction, they are obviously the ones due to a peripheral fault in the developmental morphology of the levator, failing to elevate the upper eyelid. [Figure - 1]
Bilateral cases : The 6 cases seen had, more or less a symmetrical ptosis on the two sides. There was a postural backward tilt of the head in all, the patients obtaining vision through narrowed palpebral apertures because of bilateral ptosis. [Figure - 2]A.
Visual axes retained a parallelism in all directions of the gaze in which the eyes could move in these cases. Occlusion of either eye in turn did not give rise to retraction of the upper lid of the uncovered eye. In 3 cases elevation of both the globes was normal, and in 3 others there was an absence of elevation of the globes. [Figure - 2]B.
B. Those Which Showed Areduction of the Ptosis on Occlusion of the Sound Eye
In this category I have come across only one case which has already been reported (Jain, 1957-a). It was one of unilateral congenital ptosis with an impaired function of the superior rectus. The clinical features observed in group A of the congenital cases provided reason for making a detailed clinical study of this case with a view to finding the determining cause for tile occurrence of this phenomenon. Fresh points of interest are brought out and deserve to be recorded.
Subjective Symptoms : There were no subjective symptoms of any kind, the patient complaining of no diplopia and the parents noticing no compensatory head posture.
Objective Signs : The following signs were present ;
Head posture was normal. There was no ocular torticollis.
Primary Position : There was right sided ptosis [Figure - 3]A dating from birth. The right eye was hypotropic with its visual axis directed downwards [Figure - 3]B.
Visual acuity : R. E. 6/9 and L. E. 6/6, there being no binocular vision. The left eye was the fixing eye in forward gaze.
Ocular movements : On dextroelevation, the right eye behaved in a fashion typical of a right superior rectus palsy as suggested by Bridge- man and Lyle (1957), with overaction of the left inferior oblique. [Figure - 3]C.
On laevo.elevation a typical inferior oblique palsy was indicated on the same (right) side with overaction of the left superior rectus.
[Figure - 3]E.
In all positions of elevation a complete incomitance can be seen rom [Figure - 3] (C, D and E).
Cover test : Occlusion of the left eye brought about one primary and two secondary movements. The primary movement was of a slight upward shift of the right eye so that its visual axis became horizontal to assume fixation. Two secondary movements resulted from the first-(a) the right ptosed lid was retracted, making the palpebral aperture wider, and (b) a marked up shoot of the left eye behind the cover, indicating that the secondary vertical deviation was greater than the primary vertical deviation. The retraction of the lid and the upward movement of the right eye were the same in amount on occlusion of the left eye as when testing the elevation of the globe without a cover. It follows that the sound eye moved upwards behind the cover to the same extent as it did when its elevation was tested without a cover. The width of the right palpebral aperture while testing the elevation of the globes or on occlusion of the left eye became as wide as, and never wider than, on the normal side [Figure - 4].
Experimental Observations -Two experiments were carried out :-
1.If an opaque disc was sutured to the affected eye [Figure - 5] A thus abolishing the fixation with the right eye, neither this eye nor the ptotic lid moved upwards when the left eye was covered [Figure - 5]B.With the primary movement not taking place the secondary upshoot of the covered eye did not take place either.
2.0.5 c. c. of 2.0% solution of novocaine was injected in the right superior rectus. With its action paralysed,
ptosis was enhanced ten minutes later [Figure - 5]C of [Figure - 3]A and occlusion of the left eye failed to bring about a lid retraction [Figure - 5]D.
Surgical Exploration- This was combined with surgical treatment. When explored for evidence of any abnormal muscular, fibrous or fascial connection between the superior rectus and the levator, and/or superior oblique, none were found to be present. The morphology and elasticity of the superior rectus on passive traction was normal.
Exploring the inferior fornix strong fibro-muscular connections were discovered between the inferior rectus and the inferior oblique. Near its insertion the inferior rectus was split into two slips, one normally attached
to the eyeball and the other to the inferior oblique. The inferior rectus was otherwise neither inelastic nor fibrosed
These bands between the inferior rectus and the inferior oblique were cut and the inferior rectus was recessed 5 mm. At the same time partial myectomy of the contralateral inferior oblique was performed.
Though the hypotropia of the right eye was much reduced [Figure - 6]A ptosis remained unaltered [Figure - 6]B-cf [Figure - 3]A until corrected by a Blaskoviez operation [Figure - 6]C.
C. Those Which Showed a Synkinetic Pseudo-Ptosis on Adduction and Lid Retraction on Attempted Abduction
These cases had a congenital palsy of the sixth nerve and simulated duane's Retraction Syndrome in some respects. Three cases elucidating these similarities are described by Jain (1957-b). Three new cases are described in [Figure - 7],[Figure - 8],[Figure - 9] respectively to confirm Jain's observations and show that (a) with the absence of abduction there was a tendency to widening of the palpebral aperture on attempting it, and (b) with a normal adduction, there was a tendency to narrowing of the palpebral aperture in attempting it due to pseudoptosis.
| Acquired Cases|| |
Thirty two eases were seen in all.
Seven cases (2 of head injury and one after typhoid being under 5 years of age and non co-operative for photography, and 4 others of undetermined aetiology) are not included in this paper. The remaining 25 cases were of the following nature.
A.Those Which did not Show Reduction of the Ptosis
There were 14 cases, out of which 7 were unilateral and 7 bilateral. In four cases occlusion of the sound eye did not produce a palpebral retraction. Three unilateral cases are described later [Figure - 30],[Figure - 31],[Figure - 32].
Unilateral cases : In two cases all ocular movements were completely absent. One of these had symptoms of coronary thrombosis, whereas the other had a sphenoidal fissure syndrome. In the remaining two all the movements including elevation were completely normal. One of them had an ophthalmoplegic migraine causing ptosis and the other had ptosis following tarsectomy.
Bilateral eases : All the bilateral cases showed a complete similarity in that the lid retraction on occulsion of each eye in turn, was absent. Two cases were those of progressive muscular ophthalmoplegia, four of myesthenia gravis (prostigmine positive) and one of an unknown aetiology of peculiarly interesting nature. One case of myestherlia gravis and - the one with an unknown aetiology are presented in [Figure - 10]. Those of progressive muscular oplithalmoplegia, being very similar, were non cooperative and could not be properly photographed. The second case in [Figure - 10] deserves a special mention. This female patient developed bilateral ptosis at the age of 18 years and strabismus of an incomitant nature. The condition remained stationary for 38 years without giving rise to diplopia and muscular weakness or fatigue. She was definitely prostigmine negative
B. Those Which Owedsh Retraction (Fuchs phenomenon on side to side movements and/or pseudo-Graefe phenomenon on downward gaze.)
All these cases suffered from ophthalmoplegia in the past. The ocular movements had been restored to normal with recovery (or become exaggerated owing to secondary contractures) in certain directions, or were restricted in others. Consequent upon this there had developed an altered relationship of ipsolateral and contralateral synergists and antagonists in a methodical way. In no case were all the ocular movements completely absent. The following 11 cases (including 2, already described elsewhere) out of which 10 were unilateral and one was bilateral, are placed on record to bring out important points.
Case 1 :- A female patient aged 31 years, gave a vague history of head injury in infancy. The right eye was normal in all respects, its vision being 6/6. The left eye was slightly divergent in primary position [Figure - 11]A with a vision of 2/60 due to corneal opacity. On Laevoversion, no abnormality was seen [Figure - 11]B but on dextroversion, adduction of the left eye was absent and the left palpebral aperture became definitely wider [Figure - 11]C eliciting the Fuchs phenomenon of lid retraction on attempted adduction.
Case 2 :-A boy, aged 8 years, developed the condition described below at the age of 6 years following whooping cough. In primary position there was a ptosis of the right upper lid, the right eye being divergent [Figure - 12]A. On laevoversion adduction of the right eye was absent and there was a definite tendency to widening of the right palpebral aperture [Figure - 12]B. When the right eye was abducted [Figure - 12]C there was a definite tendency to enophthalmos (of the prominence of the right eye in attempted adduction [Figure - 12]B). Elevation of the right eye was absent [Figure - 12]D. On occluding the left eye the palpebral aperture became wider [Figure - 12]E than when seen in primary position [Figure - 12]A thus simulating the congenital case of reduced ptosis on occlusion of the sound eye [Figure - 4]. The left eye, however, was abducted behind the cover. Thus this case also, strictly speaking, turned out to be one of Fuchs phenomenon of lid retraction on attempted adduction.
Case 3 :-This case [Figure - 13], a girl developed ophthalmoplegia from typhoid, already reported by Jain (1957-a), is reproduced herein. (By courtesy Editorial Committee, British Journal of Ophthalmology, Case reported by Jain, 1957-a.)
She was examined again to study the behaviour of the occluded eye behind the cover. She had ptosis of the left upper lid in primary position [Figure - 13]A. On occluding the sound right eye there was a reduction in ptosis [Figure - 13]B. Elevation of the globe was absent. On dextroversion, on attempting to adduct the left eye, lid retraction was present [Figure - 13]C. It was subsequently discovered that whereas the ptosis of the left lid got reduced on covering the sound right eye the sound eye itself got involuntarily abducted behind the cover. This produced a simultaneous attempt at adduction of the left eye leading to a secondary elevation of the ptosed lid for the purpose of obtaining vision. Thus the case which was mistaken by Jain (1957-a) to be one of paradoxical lid retraction of acquired ptosis on occlusion of the sound eye turned out to be one of Fuchs phenomenon of lid retraction on attempted adduction.
Case 4 : -This case also reported by Jain (1957-a) is reproduced below. The boy had developed a right sided ophthalmoplegia from head injury [Figure - 14].
There was ptosis on the right side [Figure - 14]A. On occlusion of the left eye there was a lid retraction [Figure - 14]B. On looking to the right ptosis increased [Figure - 14]C. Elevation of the right globe was absent and the eye was slightly abducted. Adduction of the right eye was absent and on testing it a retraction of the right lid was seen [Figure - 14]D. The pseudo-Graefe phenomenon of lid retraction was present on downward movement of the eyeball [Figure - 14]E. The left eye was normal in all respects.
Having been subjected to a detailed investigation this case showed fresh points of interest. The behaviour of the sound eye behind the cover was studied. The eye moved downwards behind the occluder, as in [Figure - 14]E, a procedure involuntarily adopted to obtain vision with the unsound eye now left open. This case, thus, turned out to be one of pseudo-Graefe phenomenon even op covering and not one of paradoxical lid retraction on occlusion of the sound eye in acquired ptosis, as stipulated by Jain (1957-a).
Experimental observation: -0.5 c.c. of 2.0% solution of novocaine was injected in the medial rectus. Observation made ten minutes later showed that ptosis was exaggerated in a manner exactly similar to the congenital case as shown in [Figure - 5]C. Reduction of ptosis causing widening of the palpebral aperture on attempted adduction of the right eye in laevoversion was much less [Figure - 15]A, ef [Figure - 14]D. The increased effort by frontalis to elevate the right upper lid is noteworthy. In dextroversion when the right eye was abducted ptosis was exaggerated [Figure - 15]B, cf [Figure - 14]C and there was an absence of effort by the frontalis to elevate the lid.
Surgical Observations:- 3 facts were noted-(a) after the external rectus was anaesthetised b) an injection of 2.0 % novocaine solution in the process of recessing the lateral rectus to correct the divergence, a passive traction on the muscle medially failed to adduct the right eye completely. This is subsequently elucidated in case 5 [Figure - 17]B. (b) After such an injection in the external rectus, divergence of the right eye was decreased and the palpebral aperture opened somewhat. This too is subsequently elucidated in case 5 [Figure - 17]C. (c) Following a recession (8 mm) of the external rectus and resection (5 mm) of the internal rectus on the right eye a marked improvement took place in the ptosis, making the two palpebral apertures equally wide [Figure - 15]C.
Case 5 : -A girl aged 18 years was a case of left sided III nerve palsy since the age of five years following hyperpyrexia. The palsy was complete. In primary position there was a complete ptosis on the left side [Figure - 16]A and the left eye was abducted behind the ptosed lid. Elevation was absent [Figure - 16]B. On dextroversion, adduction of the left eye was completely absent [Figure - 16]C, nor was there any tendency to widening of the palpebral aperture. On laevoversion ptosis was enhanced [Figure - 16]D. The comparative enophthalmic tendency of the left eye in [Figure - 16]D against its prominence in [Figure - 16]C is noteworthy. On occlusion of the right eye there was reduction in the ptosis on the left side, the eye failing to reach the mid line in its attempt to adduct but the right eye got markedly abducted behind the cover [Figure - 16]E. Thus this case showed a tendency to Fuchs phenomenon of lid retraction, elicited only when the sound eye was occluded and could have easily been mistaken for paradoxical lid retraction on occlusion of the sound eye in acquired ophthalmoplegia.
Experimental observations :- In this case the external rectus, which was in a contracted state, was temporarily paralysed by an injection of novocaine solution. There was an automatic reduction in the ptosis, the palpebral aperture was partly opened and the left eye was no longer so much abducted [Figure - 17]A. On passive traction to adduct the left eye, there was a greater widening of the palpebral aperture due to lid elevation [Figure - 17]B but adduction was still incomplete and the right eye was markedly abducted behind the cover. On laevoversion the left eye did not abduct (due to the injection) and the palpebral aperture remained wider [Figure - 17]C-cf [Figure - 16]D. On occluding the right eye a greater widening of the left palpebral aperture was noticeable than seen before [Figure - 17]D-cf [Figure - 16]E and [Figure - 17]A but the right eye got abducted behind the cover.
Case 6 :-A female, aged 16 years, developed squint in infancy following high fever Examination showed a divergent strabismus of 45 0 in the right eye, with a slight ptosis [Figure - 18]A. On dextroversion ptosis was enhanced, the palpebral aperture became narrower and there was tendency to enophthalmos on the right side [Figure - 18]B. On attempting adduction of the right eye there was a widening of the palpebral fissure, an increased prominence of the right eye and the paralytic nature of the strabismus was evident in the incomitance of the eyes [Figure - 18]C. Thus the case turned out to be one of Fuchs phenomenon of lid retraction on adduction.
Surgical observations :-The right and left external recti were recessed 7 mm. each and the right internal rectus was resected 6 mm. at the same time. The result two months after the operation is shown in [Figure - 19].
Divergence of the right eye was considerably reduced [Figure - 19]A, abduction of the right eye no longer gave rise to pseudo- ptosis [Figure - 19]B and widening of the palpebral aperture was abolished [Figure - 19] C on adduction of the right eye.
Case 7 :-Male aged 41years, showed a pseudo-Graefe phenomenon of lid retraction on the left side on downward gaze [Figure - 20]D. All ocular movements were normal. History revealed a tendency to intermittent rise in his blood pressure in the past (though when examined recently it was 135/80), intermittent bleeding from the nose since childhood and from pyorrhoeic gums now. In 1935 he suffered from pain and swelling in the neck just above the inner third of the left clavicle and was diagnosed as, and treated for, haemorrhage following venous thrombosis at the root of the neck of the left side. In January 1957 he had attacks of paroxysmal cough and haemoptysis from which he recovered. [Figure - 20] shows the relevant features.
Case 8 :-Female, aged 17 years, sustained a serious head injury from a fall on a hard floor in 1955. There was bleeding from the nose and the mouth, a large haematoma had formed in the left temporal region, blood and high tension was discovered in the cerebrospinal fluid on lumber puncture. Examination of the eyes then showed a contracted pupil on the right side and a dilated fixed pupil on the left. 'There was also a haematoma in the root of the neck due to a clavicular fracture on the left. Extradural and subdural clots were removed through trephine holes in the left parietal region. Fifteen days later a complete third nerve palsy was discovered on the left side.
Examined on 28th October 1957 vision in each eye was 6/24 and corrected with glasses it was 6/6. though the left pupil was widely dilated and fixed. In primary position there was a slight ptosis on the left side [Figure - 21]A but adduction was normal [Figure - 21]B. On adducted depression, however, a pseudo-Graefe phenomenon developed on the left side [Figure - 21]C. A slight limitation of abduction of the left eye was present on laevoversion [Figure - 21]D.
Case 9 :-Male, aged 10 years, following a blunt injury to the right upper lid in 1948, developed a swelling of the right eyes. With time as the swelling subsided ptosis appeared on the right side [Figure - 22]A and the eye became hypotropic. On dextroversion abduction of the right eye was normal [Figure - 22]B and palpebral aperture became wider. Elevation of the right eye was absent and ptosis remained unaltered [Figure - 22]C at one time, and at another the right upper lid showed a smasmodic retraction [Figure - 22]D. On occlusion of the left eye sometimes there was no tendency to retraction [Figure - 22]E and yet sometimes in the abducted [Figure - 22]F or adducted [Figure - 22]G positions of the right globe a spasmodic involuntary lid retraction opened the palpebral aperture.
Surgical observation :-Blaskoviez operation was performed. At one time a fairly symmetrical appearance was restored [Figure - 23]A At another a spasmodic lid retraction made the right palpebral aperture much wider than the normal side [Figure - 23]B, and on occlusion of the sound eye an exaggerated lid retraction, was sometimes noticeable on the right side [Figure - 23]C.
Case 10 :-Male, aged 65 years, being a diabetic and hypertensive (B. P. 185/105) developed a palsy of the right external rectus. On dextroversion while attempting abduction of the right eye there was a widening of the palpebral aperture [Figure - 24]A, the appearance on laevoversion being normal [Figure - 24]B.
Case 11 :-This was the only bilateral case seen. A male, aged 46 years developed a bilateral palsy of the external rectus following a severe attack of neuralgic type of headache on the right side.
Fundi, skiagram of the skull, general neurological examination by a physician and the laboratory investigations were negative (lumber puncture was not permitted). In primary position with the right eye fixing, the left eye was convergent [Figure - 25]A and with the left eye fixing, the right was convergent [Figure - 25]B and the left palpebral aperture became wider due to lid elevation. On dextroversion [Figure - 25]C and laevoversion [Figure - 25]D abduction was restricted on either side with a well marked lid retraction, that on the left being more than the right. On a downward gaze a pseudo-Graefe phenomenon was present on the left side [Figure - 25]E.
Experimental observation :- Novocaine was injected in the left external rectus. On laevoversion [Figure - 26]-note conjunctival chemosis after injection) the left eye could not abduct at all, as against a slight abduction which was possible before such an injection (cf [Figure - 25]D). Though the excessive nervous effort originating in the paresed left external rectus was abolished the lid retraction on attempted abduction remained persistent on the left side.
Observations after recovery (4 month later)- Absolute normality was restored in all positions of the eyes [Figure - 27].
| Exophthalmometry|| |
As more and more cases of pseudoptosis and palpebral retraction were studied both being inversely related to each other, in congenital and acquired ophthalmoplegias two facts were discovered-(a) a relative enophthalmos taking place when the eyeball moved in the direction of a contracted (i.e. stronger) muscle thus enhancing the ptosis, and (b) a relative prominence of the eyeball when a movement was attempted in the direction of the paresed muscle which gave rise to reduction in the ptosis. Thus the possibility of an antero-posterior ocular displacement occurring in acquired cases gave the idea that ocular retraction was not a feature typical only of Duane's Retraction Syndrome but also of some cases of congenital lateral rectus palsy as well as of acquired ophthalmoplegia of the horizontally acting muscles. The next question was "Which were these cases ?", and it was discovered that such an ocular displacement was noticeable to the naked eye only in cases wherein both pseudo-ptosis and lid retraction were present alternately in opposite movements of the same eye i.e. if in one direction pseudoptosis occurred lid retraction disappeared and in the opposite direction of the ocular movement pseudo-ptosis disappeared with the occurrence of lid retraction. The statements are proved by the study of exophthalmometric readings hereunder.
METHOD OF RECORDING :-Readings (in mm.) were recorded in abducted, forward and adducted positions of each eye. Allowing for the possibility of a small degree of objective error in recording the exophthalmometric findings inferences can be drawn with a fair degree of accuracy, particularly where the difference in readings in different positions of the gaze is more than 2 mm. A difference of about 1 mm. may be considered statistically insignificant. For the sake of convenience a style in arrows (pointing outwards to signify abduction, straight down to signify a forward gaze and inwards to signify adduction) will be adopted for each eye shown in [Figure - 28] and the exophthalmometric reading placed at the head of the arrow. Dotted lines will be used in the affected eye to signify a paresed muscle and a thicker line the contracted overacting muscle. For example, in a lateral rectus palsy of the left eye the exophthalmometric readings in various positions of the eyes will be indicated in a fashion shown in [Figure - 29].
I. Exophthalmometric readings in congenital lateral rectus palsy :- Findings in four cases are summarised in [Table - 1].
In all cases there was (a) a tendency to widening of the palpebral aperture when the eye tended to move in the direction of the paresed muscle i.e. in the direction of the dotted lines in the above table), and (b) a tendency to narrowing of the palpebral aperture in the direction of the stronger contracted muscle (i.e. in the direction of the thick line in the [Table - 1]).
II. Readings in acquired medial rectus palsy :--These were recorded under 2 groups.
A.Cases, wherein widening of the palpebral fissure was present when the eye tended to move in the direction of the paresed medial rectus and narrowing occurred when the eye moved in the direction of the secondarily contracted lateral rectus. [Table - 2].
Regarding case 2 in the [Table - 2] (case 8 of this series) it may be pointed out here that at the time of recording the exophthalmometric readings no palsy of the medial rectus was noticeable (though at the time of the head injury it was there) but a residual paresis of the left external rectus was present [Figure - 21]D and yet there was a widening of the palpebral aperture in adducted-depression of the left eye to elicit a pseudo-Graefe phenomenon [Figure - 21]C.
B. Wherein widening of the palpaberal aperture was absent -one left sided case (male, 26 years) of one week duration is illustrated in [Figure - 30] and its exophthalmometric readings are recorded in [Table - 3], which, in this instance, revealed no difference in the exophthalmometric readings in the adducted and abducted positions of the affected eye. He gave a positive history of syphilis and the serological test of the blood for syphilis was positive.
It is to be noted that in attempted adduction of the left eye, which was absent, there was perhaps a slight tendency to widening of the palpebral aperture [Figure - 30]B, but definitely no tendency to narrowing by pseudoptosis in abduction [Figure - 30]C.
III. Readings in acquired sixth nerve palsy :-
A. Wherein lid retraction was present-two cases (No. 10 and No. 11) were measured [Table - 4].
B. Wherein lid retraction was absent-Two cases were examined.
One ease (male, 45 years) had a bilateral sixth nerve palsy since one month, after an acute attack of headache. No widening or narrowing of the palpebral fissure was present on side to side movements [Figure - 31]. Exophthalmetric readings are recorded in [Table - 5].
The other case (male, 10 years) developed a left sided sixth nerve paresis following left mastoidectomy done three weeks ago [Figure - 32]. No widening or narrowing of the palpebral fissure was noted. [Table - 6] shows the exophthalmometric readings.
IV. Readings in 15 cases of concomitant squint are summarised in [Table - 7]. No abnormal ocular displacement or lid movement was present in these cases. Though a difference of 1 mm in the readings in various directions of the gaze was noticed due to unexplained reasons, as has been pointed out before (p 17) this can be statistically disregarded.
| Discussion|| |
Elevation of the Ptosed Lid N Occlusion of the Sound Eye
1.0 Congenital Cases
(1)Type of Cases in Which this Pnenomenon was not Seen :-
Unilateral cases-Those in which the function of the superior rectus was absolutely normal, the elevation of the globe being maximal, this phenomenon was not seen. These cases resulted from a peripheral fault in the development of the levator only [Figure - 1].
None of the bilateral cases showed an elevation of the lid. Those which had a normal elevation of the globes [Figure - 2]A had a congenital fault in the morphology of the levator, like the unilateral cases, the superior rectus having been spared. Those which, aside from ptosis, also showed an absence of elevation of the eyeballs [Figure - 2]B were presumably due to a congenital nonseparation of the superior rectus and the levator in the process of embryological differenciation.
It is possible that even a unilateral case with an absence of elevation of the globe may not show elevation of the ptotic lid, though the author himself has not yet recorded a similar case. This would, presumably, be due to a similar congenital nonseparation of the levator and the superior rectus on one side alone.
(2) Study of the Case Which Showed this Phenomenon :-
In this case elevation of the eye was restricted but not completely absent or completely normal. When
its fixation reflex was abolished [Figure - 5]A, the palpebral elevation did not take place to open the eye [Figure - 5]B. It is possible, therefore, that the ptotic lid on the side of an eye previously blinded may, under otherwise exactly identical circumstances, not show an identical elevation of the ptotic lid.
Absolute inactivity of the superior rectus, temporarily and artificially created, did not permit the occurrence of this phenomenon [Figure - 5]C and D. Not only did it prevent retraction but it actually favoured ptosis [Figure - 5]C and this proves the closely linked synergic action of the superior rectus and the levator. Thus the real predisposing factor in the occurrence of this phenomenon appeared to lie in the underaction of the superior rectus.
Menacho (1917) in his statement that no purely anatomical explanation could explain the occurrence of the cases which were not congenital, but were acquired, indicated the possibility of an anatomical basis for the congenital cases. The presence of a congenital fibromuscular band between the inferior rectus and the inferior oblique in this case supports this, and suggests an infranuclear aetiology. It is not surprising that such a band was discovered in vivo, since Fink (1948) has demonstrated a similar discovery in respect of the ligament of Lookwood in cadavers.
In normal individuals as both the eyes elevate themselves from a hypotropic position so do the upper eyelids also get elevated proportionately from a drooping position. In the congenital ease showing this phenomenon the eye on the effected side elevated itself upto a point and so did the eyelid. At a certain level such a movement, both of the eyeball and the eyelid, got arrested by a mechanical interference, those on the unaffected side proceeding unhampered. This band, probably, rendered the inferior rectus in such a state of inexpansile contracture as would hold back the eye from being elevated and interfere with the elevatory function of the inferior oblique. Thus, the mechanism on the affected side appeared to have got reversed from the acquired cases in that the primary lesion lay in the contracted state of the inferior rectus leading to a secondary mechanical inhibition of the ipsolateral antagonists, the superior rectus, the inferior oblique and the levator, all the three being embryologically, neurologically and functionally synergic in nature.
Significace of Socclusion:-
Occlusion of the sound eye did not seem to contribute towards the occurrence of the lid retraction, but by putting the sound eye out of function, it merely forced the affected eye to assume fixation. With the abortive action of the superior rectus to move the eye upwards an equal and reciprocal stimulation of the levator caused the lid to be elevated partially. The width of the palpebral aperture on the affected side on occlusion of the sound eye or when elevation of both eyes was tested without occlusion became equal to the normal side seen in primary position, but never wider than the normal side. This indicates that the levator was not over stimulated through a voluntary overflow of impulses from superior rectus.
Site of Lesion :-
The most commonly accepted hypothesis (Duke. Elder, 1952-a) for the occurrence of this phenomenon is one of an abnormal nervous connection existing in the central nervous system between the neive supply of the levator and the associated muscle, there being no complete explanation to elucidate the rationale of these associated movements.
The incomitant nature of the vertical strabismus [Figure - 3] shows that the aetiological mechanism cannot be attributed to supranuclear dissociations since the disturbance in the motility of both the eyes was neither equal nor simultaneous.
The question of a congenital maldevelopment taking place so as to involve the nucleus of the levator causing ptosis, as well as those of the superior rectus and the inferior oblique, causing absolute absence of elevation of the globe [Figure - 3] does not seem to be likely. To expect an absolute normality of the other components of the third nerve nucleus with an isolated congenital dysfunction of the nucleus of the levator, the superior rectus and inferior the oblique on one side, without influencing the contralateral side through crossed fibres, does not sound to be rational.
In the absence of any other better explanation, the question of aberrant neurological interconnections, at least in identical cases, becomes debatable.
These observations emphasize the need for observing the behaviour of the occluded eye behind the cover to avoid certain mistakes.
II. Acquired Cases
Lid elevation on the side of ptosis in acquired cases on occlusion of the sound eye took place in all the cases which showed a Fuchs phenomenon of lid retraction on attempted adduction in third nerve palsy (cases 2, 3, 4, 5 and 10).
Occlusion of the sound eye in acquired cases, like the congenital case, had nothing to contribute towards the occurrence of such a phenomenon directly. It merely forced the affected eye to assume fixation. The primary horizontal movement of attempted adduction brought about two secondary movements-(a) exaggerated synergic action of the levator which lifted the ptotic lid to enable the unsound eye to obtain vision, (b) an increased abduction of the sound eye behind the cover, because the angle of secondary horizontal deviation was greater than that of the primary deviation.
This further emphasises the need for observing the behaviour of the sound eye behind the cover before any conclusions as to the nature of the palpebral elevation can be drawn.
Mistakes in the interpretations were made by Jain (in reporting cases 2 and 3, 1957-a) because of this lack of observation. This mistake is demonstrated in cases 2 and 5 [Figure - 12]E and [Figure - 16]E respectively). It may be stated that a similar mistake could also have been repeated in cases 1 and 6 if in [Figure - 11]C and [Figure - 18]C respectively the sound eye had been kept occluded and the lid retraction alone of the paresed eye had been noted. Thus, these two cases could easily have been photographed to elicit an elevation of the ptotic lid on occlusion of the sound eye and reported upon. A similar phenomenon could also be demonstrated in case 11 of the external rectus palsy if in [Figure - 25]D the right eye had been occluded and the case photographed.
These observations indicate that the, so called, cases of paradoxical lid retraction on occlusion of the sound eye in acquired ptosis are really the ones of Fuchs phenomenon of lid retraction on attempted adduction of the affected eye. In Yanes' case (1940) this phenomenon was elucidated by screening the sound eye with the hand of the subject. It is quite likely that the behaviour of the covered eye was not studied, which may well have been abducted behind the cover.Completeclinicalislackingbuttheillustrationsindicateasimplethird nerve palsy, simulating cases 2, 3, 4, 5 and 10 of this series. It seems correct, therefore, to assume that, perhaps, Vanes case was also one of Fuchs phenomenon of lid retraction and not one of paradoxical lid retraction on occlusion of the sound eye.
Cases described under the heading of "Those which did not show retraction" indicate that the phenomenon of lid elevation did not take place in the following circumstances of ptosis (a) when the ocular movements were completely normal in all directions, (b) when the ocular movements were completely absent in all directions, and (c) progressive degenerative lesions affecting the oculomotor nuclei or the extraocular muscles.
It has been suggested by Duke. Elder (1952-b) that such a phenomenon indicates a sensory-motor association at high level. This was based on the cases of neurosyphilis reported by Gifford (1939) and Yanes (1940). The similarity, at least of Yanes' case, with the cases described in this paper, has been demonstrated. From the association of this phenomenon with that of the Fuchs phenomenon of lid retraction on side to side movements of the eyeball, it is reasonable to conclude that there is no such independent entity of lid retraction on occlusion of the sound eye. Where Fuchs phenomenon was not present this too was absent.
| Fuchs Phenomenon of Lid Retraction on Side to Side Movements|| |
This phenomenon was observed where either the medial rectus or the lateral rectus was paresed.
I. In Medial Rectus Palsy :-
Secondary to such a palsy contracture of the antagonists and inhibitional palsy of the synergists was present in a methodical way.
A. Inference from Novocaine Injection in the Medial Rectus :-
Abolition of excessive nervous effort originating in the paresed medial rectus, thus brought about, reduced Fuchs phenomenon of lid retraction on attempted adduction [Figure - 15]B.
By such a measure ptosis was enhanced in primary and abducted positions of the globe [Figure - 15]B cf [Figure - 14]C thereby indicating that the adductive power of the medial rectus favoured opening of the palpebral aperture. It is, perhaps, correct to assume the presence of a synergic relationship between the medial rectus and the levator. Such an injection rendered the external rectus relatively stronger than the medial rectus. Thus the excessive effort on the part of the external rectus cannot be considered as a likely cause for the occurrence of Fuchs phenomenon on abduction.
B. Inference from Novocaine Injection in the External Rectus
This favoured a slightly better adductive effort by the paresed medial rectus and gave rise to an automatic elevation of the ptosed lid, the palpebral fissure becoming wider than before in all positions of the globe [Figure - 17]A, C and D.
This further supports the statement of a direct inter-relationship between the medial rectus and the levator, and an inverse relationship between the actions of the external rectus and the levator.
C. Inference from Passive Traction :-
In cases 4 and 5 this was done and two observations were made (a) the eye could not be fully adducted on passive traction medially and (b) the palpebral fissure became wider [Figure - 17]B. The reason for the first appears to lie in the marked contracture of the external rectus, thus rendered inelastic due to an old standing palsy of filo, medial rectus. This situation is analogous to the one playing an important aetiological role in the causation of Duane's Retraction Syndrome (Nutt, 1955 and Jain 1957-b).
The second discovery lends further support to the observations of a direct corelation in the behaviour of the medial rectus and the levator.
D. Inference from Surgical Experience :-
Judging from the inferences made from experimental study of the cases it seemed reasonable to expect restoration of normality in the behaviour of the ptosed lid if parallelism of the visual axes of the two eyes Mere to be restored in the horizontal plane.
With this argument in mind the paralytic horizontal strabismus in cases 4 and 6 was surgically corrected. With the reduction of divergence of the affected eye ptosis was markedly improved [Figure - 15]C and [Figure - 19]A respectively), the palpebral fissure becoming almost equal on the two sides. Abolition of Fuchs phenomenon of lid retraction on attempted adduction [Figure - 19]C is noteworthy.
That restoration of parallelism of the visual axes restored normality in the behaviour of the eyelids, even with conservative treatment, where possible, can be judged from case 11.
Gowers (1883) suggested the possibility of the involuntary stimulation carried by one nerve from its usual channels into another i.e. from the medial rectus to the levator. The view seems to find its support from Fuchs' case (1895) of syphilis and Cord's case (1930) of trauma. The points brought out from the experimental and surgical observations dispute the view. A direct close synergic type of action between the medial rectus and the levator is demonstrated, If the medial rectus contracted, the levator also acted and vice versa. Judging from the law of equal and reciprocal innervation in the case of paresis the response of the medial rectus to a stimulus would be poor but to such a stimulation, there being an equal stimulation of the levator, the levator would respond effectively, thus showing a lid elevation. Whereas, the stimulation has to be far in excess of the response obtained from the paresed medial rectus, the response of the levator is proportionate to the same excessive synergic stimulation and hence the apparent lid retraction.
To every primary movement there must be a secondary movement, like the angle of the primary and secondary deviation. To such a primary movement of the paresed medial rectus, aside from the exaggerated secondary deviation of the sound eye brought about by the contralateral synergists, there is also an overaction of the ipsolateral synergist, the levator being akin to the latter. Thus Fuchs' view (1895), in the central nervous system, and Bielschowsky's view (1932-35), in the periphery of the wandering of regenerating axons out of their usual tracts into strange but neighbouring pathways do not seem to be based on proofs.
Establishment of parallelism of the visual axes of the two eyes surgically (cases 4 and 6) led to the abolition of the phenomenon of lid elevation. The question of a neurological interconnection having got established in the event of a paresis, and disappearing after a balance was struck in the amplitude of action of the synergists and the antagonists, can not be agreed upon as being correct. Similarly the question of straying of nerve fibres from the sheath of one into that of others as suggested by Bender (1936) also becomes doubtful.
II. In External Rectus Palsy :-
A. Congenital :-
As a congenital lesion a spasmodic elevation of the lid on the side of the contracting muscle has been observed by Pfluger (1892), Friedenwald (1893- 96), Fuchs (1895), Brixa (1898), Marlyn (1919), Bielschowsky (1932) and Jain (1957-b). It is a well known occurrence in Duane's Retraction Syndrome. In this series three cases of congenital palsy of the external rectus [Figure - 7],[Figure - 8],[Figure - 9] showed a similar retraction. Jain's argument (1957-b) of the absence of a nuclear interconnection through regeneration of aberrant fibres from the nucleus of the sixth nerve into that of the levator, seem to indicate a peripheral cause for the occurrence of the lid elevation with attempted abduction in this group of cases.
The question of amplitude of the greater secondary movement (i.e. the levator action in producing lid elevation) in response to a restricted primary movement of abduction (i.e. the limited action of the paresed external rectus) does not apply to these cases, as it does to cases of medial rectus palsy mentioned before, because an inverse relationship is in existence between the external rectus and the levator as demonstrated in acquired cases (5 and 11). If there is no directly interlinked connection between the two, the cause of this synkinesis must be different.
B. Acquired ;-
As an acquired lesion, the phenomenon has been observed to result from meningitis by Wilbrand and Saenger (1900-21), and syphilis by Jain (case 4, 1957-a). In case 11 of this series the same was observed. It was not abolished with the abolition of excessive nervous effort of the paresed external rectus [Figure - 26] by injecting novocaine in it. This further shows that the overaction of the paresed external rectus in no way influences the behaviour of the lid, a point raised above. If the origin of the phenomenon lay in the external rectus wherefrom excessive impulses were transmitted to the levator, such a lid retraction from levator action ought to get abolished. The cause must, therefore, lie else where since an inverse relationship between the lateral rectus and the levator has been demonstrated earlier.
| Pseudo-Graefe Phenomenon of Lid Retraction on Down-Ward Gaze|| |
Several factors, single or combined appear to play an important aetiological role in the occurrence of such a phenomenon.
A. The Role of the Sympathetic Stimulation :-
The example of case 7 [Figure - 20]D illustrates the irritation of the cervcial sympathetic as an isolated cause for giving rise to such a lid retraction, since there was no cranial cause for ophthalmoplegia.
Case 8 [Figure - 21]C, being of a mixed nature, had a cranial cause for the ophthalmoplegia, as well as an irritative cause for the cervical sympathetic due to fracture of the clavicle which may have contributed to retraction.
What explains the occurrence of bilateral sixth nerve palsy, in case 11 due, probably, to some cause at the base of the skull, and the associated pseudo-Graefe phenomenon is uncertain. From the arguments raised for explaining the occurrence of lid retraction associated with paresis of the external rectus it is possible that the sympathetic stimulation at the base of the skull may have something to do with an irritative lid retraction in this case. This may also explain its occurrence, particularly in the absence of a direct neurological interconnection between the lateral rectus and the levator, in all traumatic cases and cases of cerebral neoplasms (Bender, 1936) intracranial aneurysms (Walsh and King, 1942), anterior poliomyelitis (Fortuyn, 1899), tabes (Fuchs, 1895), vascular lesions in the brainstem (Koppen, 1894), subarachnoid hamorrhage and trauma (cases 1 & 3 respectively reported by Jain, 1947-a), etc. The role of sympathetic stimulation in Claude Bernard's Syndrome (1852) is well known in the lid retraction.
It is generally maintained that the Fuchs phenomenon of lid retraction on side to side movements is found in palsies of old standing when a state of recovery sets in. In cases 10 and 11 retraction, was present from the very beginntion which disappeared completely in four months time with recovery in the latter. In this variety of cases, therefore, the statement does not apply. This also lends support to the possiblity of a different cause operating herein, such as an irritation of the sympathetic.
B. The Role of Medial and Lateral Recti:-
Bielschowsky's case (1932-35) and case 8 of this series show a similarity in the fact that this phenomenon was most markedly evident in the movement down and in than down and out (pointed by Duke-Elder, 1952-c). The latter movement Is aided by the sixth nerve, whereas the former by the internal rectus. It suggests that the action of the medial rectus contributes to such a phenomenon and it is possible that when associated with the movement down and out, in which the external rectus is concerned, there may be some other causative influence, for example the sympathetic.
Whether in association with the lid retraction in attempted adduction in medial rectus palsy and a pseudo-Graefe phenomenon there is an absence of paresis of the external rectus (case 4), or there is a presence of external rectus palsy (case 8), one fact stands out significantly that the external rectus does not influence the behaviour of the upper eyelid in giving rise to retraction.
The Significance of Ptosis:-
Duke-Elder (1952-d) says that lid retraction with depression of the eyes occurs preferentially when paresis of the lid is less marked than that of the oculo motor muscles simultaneously called into play. Bender (1936) says that it may occur after ptosis has recovered and voluntary closure of the lids is possible.
In the experimental (cases 4 and 5) and surgical (cases 4 and 6) study in this series, ptosis was discovered to have got markedly reduced when the visual axes of the two eyes were brought to a greater parallelism. These observations suggest that in the neurological lesions giving rise to ptosis in association with ophthalmoplegias either the levator escapes being paralysed or is first to recover from the lesion. In all such cases showing lid retraction therefore, the resulting ptosis must be pseudo and not true in nature, which gets exaggerated with the ocular movements taking place in the direction of the contracted muscle, getting reduced with the ocular movement in the direction of the paresed muscle, and disappearing when a balance in the amplitude of action of the contracted and paresed muscle is established surgically (cases 4 and 6).
Ptosis would be considered as true only when restoration of parallelism of the visual axes of the two eyes fails to improve it. Such a ptotic lid would not show retraction under any circumstances indicating a permanent damage to the levator, its nerve or the nucleus.
Halpern (1934) reported a traumatic case involving the levator nerve alone and causing ptosis, wherein this lid developed a paradoxical elevation as the ptosis disappeared. Case 9 of this series is one of a similar nature. These two cases support the statement that a recovered levator is necessary for a synkinetic retraction.
The likely explanation is that in the most initial and acute phase of the ophthalmoplegia the clinical picture of the case becomes complex due to multiple factors. When, in the course of recovery, the pressing factors secondarily affecting the nerve to the levator get withdrawn leaving behind the primary basic anomaly of a permanent nature, either the adductor palsy or the sympathetic irritation, such a phenomenon becomes manifest.
| Value of Exophthalmometry|| |
Comparing the exophthalmometric readings in the cases which did not show widening or narrowing of the palpebral aperture (those described under the groups IIB, IIIB, IV and V), with those wherein these phenomena were present (groups I, IIA and IIIA), one definite difference can be seen in the readings. Whereas in the cases which showed no abnormality the exoplithalmometric readings were, more or less, symmetrical on each side [Table - 3],[Table - 5],[Table - 6],[Table - 7],[Table - 8], those in the cases with lid retraction showed a definite asymmetry in the following two manners :-
1. In medial rectus palsy-The least reading in the affected eye was recorded when the eye ball moved in the direction of the overacting antagonist, i.e., the external rectus. The maximum reading in the affected eye was recorded when the eye attempted to move in the direction of the paresed muscle, i.e., the internal rectus, but could not do so. The statements are easily understood from [Table - 9] by summarising the observations made in [Table - 2].
2. In external rectus palsy-Likewise, in both the congenital, as well as, the acquired cases of lateral rectus palsy where there was prominence on side-to-side rotation the least readings were recorded when the eyeball moved in the direction of the overacting antagonist, i.e., the medial rectus, the maximum readings being when the eye attempted to move in the direction of the paresed external rectus. The summary of these readings proves the above statement [Table - 10].
Thus it can be seen from [Table - 9],[Table - 10] that the average anteroposterier displacement of the eyeball was approximately 3mm in side to side movements, the least reading indicating a phase of ocular retraction and the maximum indicating an increased ocular prominence. On inspection such a displacement was apparent in at least 3 cases (Nos. 2, 5 and 6).
| Significance of Ocular Displacement|| |
The normally permitted forward and backward translatory movements of the eyeball are small (Duke-Elder, 1946-e). On forcible widening of the palpebral aperture a forward displacement of 1.0 mm is reported by J. Muller (1868) and of 0.8 mm by Tuyl (1901). A converse backward displacement is reported on contraction of the lids by Donders (1871).
Under several artificially created circumstances an ocular prominence (upto 3mm) has been recorded in normal individuals by Danders (1871), Tuyl (1901), Barkan (1915) and Copper (1948). Conversely, an enophthalmos has been noticed after shortening of a particular muscle after advancement or resection, and on moving an eye after fixing it with forceps (Turk 1899).
An ocular retraction is a feature well known of the Retraction Syndrome. But in all the cases of lid elevation and increased pseudo ptosis with side to side movements described in this paper the most significant finding, was one of an identical ocular displacement. The abolition of this displacement in ease 6 after surgery [Table - 2] and in case 11 after recovery [Table - 4] was an interesting discovery. This finding places these cases in line with the lid retraction and exophthalmos met with in Claude Bernard's Syndrome (1852), though the cause may be different.
Plausible Explanation of Ocular Displacement in Ophthalmopegias :-
Several factors seem to contribute towards the ocular displacement in ophthalmoplegias. In normal individuals the retracting influence of the recti is opposed by the protracting influence of the obliques to a certain extent (Duke-Elder, 1946-c).
In paresis of a rectus whenever the paresed muscle tries to pull the eye in its own line of action two things happen--(a) it fails to do so because of the paresis, and (b) the ipsolateral antagonist relaxes very completely. It is conceivable, therefore, that in such an attempted action the retracting influence of the recti is altogether abolished and only the protracting influence of the obliques is operative in giving rise to an increased prominence of the eye. Conversely, the excessive retracting influence of the overacting antagonistic rectus, when the eye is moved in its direction, can be expected to give rise to a backward ocular displacement.
Duke-Elder (1946-f) says that in normal individuals the voluntary conjugate movements are controlled as a unity as if the two were combined in a single central organ. In paralytic squints such a control is lost and the parallel movements in the two eyes are no longer controlled as a unity, there being a disruption in the cojugate innervation.
The consideration of the mechanics of ocular movements, which is built entirely around a hypothetical centre in normal individuals seems to get altered in paretic cases. In the latter the active movements, do not remain essentially rotatory and no longer take place around the hypothetical centre of rotation. Moved in the direction of the overacting contracted muscle the eyeball may get so dragged that its centre of rotation shifts from is original place.
Mechanics of Ocular Displacement in Ophthalmoplegias:-
A diagrammatic explanation of this mechanism is offered in [Figure - 33]. This illustrates the manner in which the right eye with a medial rectus palsy or the left with a lateral rectus palsy is likely to rotate, shift forward while moving in the direction of the paresed muscle and retract while moving in the direction of the contracted muscle. It also illustrates the manner in which an equal expenditure of the impulses producing an unequal balance of the physiological forces may result in an antero-posterior ocular displacement.
Corresponding to the method employed in exophthalmometry an eye made in dotted fashion represents its position when moved in the direction of the paresed muscle and an eye made in thicker lines represents its position when moved in the direction of the contracted antagonist.
"A" denotes the visual axis of the affected eye in primary position (being slightly abducted in right medial rectus palsy or adducted in left external rectus palsy) with a centre "ca", posterior pole "PP" and a horizontal tangential plane from its anterior surface "a".
Following paresis on one side there is an unequal distribution of the physiological forces in the two eyes, that on the normal side rotating at its original centre In dextroversion this disruption shifts the fulcrum towards the posterior pole "PP" and the eye moves to position "B". The centre of the eye shifts to "cb", its horizontal plane from the anterior surface receding to "b" and signifying ocular retraction. At this position there is an increased pseudo-ptosis and narrowing of the palpebral aperture.
In laevoversion the paresed muscle fails to move the eye to the same extent as in dextroversion. The eye assumes a position at "C", again the fulcrum shifting to the posterior pole "PP" and its centre shifts to "cc". Owing to the complete relaxation of the contracted muscle, the paresed muscle already being weak, the eyeball shifts forwards with the horizontal plane from the anterior surface marked "c". This gives the eye a more prominent look.
The difference between "b" and "c" signifies the amplitude of ocular displacement, which, in these investigations, has been found to be approximately 3 mm.
The posterior pole "PP" may not necessarily be a fixed point of fulcrum of the eye in the three positions (A, B C). With the retracting influence of the recti it may shift backwards and with the protracting influence of the obliques it may shift forwards.
In this manner the mechanism of the synkinetic oculopalpebral movements in the horizontal plane can be explained by fn . nvilating a 'Law of Inverse Ocuo-Palplebral Rezraction ' as follows :-
"In an eye with a palsy of one of the horixontally acting muscles (a) if there is an increased narrowing of the palpebral aperture resulting from pseudoptosis, it is due to ocular retraction taking place when the eye moves in the direction of the contracted muscle, and (b) if there is an increased widening of the palpebral aperture owing to lid elevation it is due to a forward displacement of the globe taking place when the eye attempts to move in the direction of of the paresed muscle".
| Comments|| |
Many theories to explain the aetiology of these phenomena are disputed by offering a peripheral mechanical explanation in the orbit to exclude the aberrant supranuclear, nuclear and infranuclear neurological interconnections. The data are yet too meagre and difficulties many because the patients neither subject themselves to experimentation nor, even, surgery.
New discoveries and important facts emerging from the study of the eases described in this paper deserve a special comment.
(1) Experimental proofs are supplied to elucidate the peripheral aetiological influences in cases of medical rectus palsy.
(2) An antero posterior ocular displacement is demonstrated exophtalmometrically in acquired medial and lateral rectus palsy akin to that taking place in congenital lateral rectus palsy wherein lid retraction causing widening of the palpebral aperture is present to show a similarity in the acquired and the congenital cases.
(3) The occurrence of lid retraction on occlusion of the sound eye both in congenital and acquired cases is disputed as having a doubtful clinical significance. This is explained by :
(a) the retraction being an exaggerated secondary lid movement in response to a weak primary ocular movement, whether vertical or horizontal,
(b) the essential and invariable accompaniment of Fuchs phenomenon of lid retraction on attempted adduction in medial rectus palsy with the phenomenon of lid elevation on occlusion of the sound eye in acquired cases, indicating that the former is not an independent clinical entity,
(c) Pointing out the mistake commonly made in arriving at conclusions by the authors in the past in not studying the behaviour of the occluded eye behind the cover.
(4) A direct synergic relationship between the medial rectus and the levator is demonstrated.
(5) A detailed study of a congenital case in which lid retraction occurred on occlusion of the sound eye is reported to record the discovery of such a fibromuscular ligament of Lockwood in vivo as to have a mechanical influence in the occurrence of this phenomenon, thus giving an anatomical basis to the aetiology.
(6) The importance of sympathetic stimulation in the causation of pseudo-Graefe phenomenon of lid retraction on downward gaze and lid retraction associated with acquired sixth nerve palsy is emphasised.
(7) A "Law of inverse oculo-palpebral retraction" is suggested and explained to elucidate the synkinesis in cases of lid retraction resulting on side to side movements of the eyeball.
| Summary|| |
A study of 61 cases of ptosis and/or ophthalmoplegia (29 congenital and 32 acquired) is made. Conclusions from these and a study of 39 cases in which exophthalmometry was done, are commented upon. New explanations for the occurrence of the synkinetic oculopalpebral movements are offered.
| References|| |
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[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11], [Figure - 12], [Figure - 13], [Figure - 14], [Figure - 15], [Figure - 16], [Figure - 17], [Figure - 18], [Figure - 19], [Figure - 20], [Figure - 21], [Figure - 22], [Figure - 23], [Figure - 24], [Figure - 25], [Figure - 26], [Figure - 27], [Figure - 28], [Figure - 29], [Figure - 30], [Figure - 31], [Figure - 32], [Figure - 33]
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8], [Table - 9], [Table - 10]