Lecture: Superior Oblique Palsy: An Illustrative Guide to Management with Case Examples

This talk would give a short introduction on the etiology and assessment of superior oblique palsy. Following this, I will be showcasing 7 to 8 case examples including those with congenital and acquired onsets, all of whom I had operated upon, detailing the pre operative assessments, indications for surgery, types of surgeries done and post operative outcomes. Videos of surgeries performed would be included. At the end of the talk, the attendees would have a better insight on the management protocols of cases with superior oblique palsy.

Lecturer: Dr. Sandra Ganesh, Consultant, Department of Paediatric Ophthalmology and Strabismus, Aravind Eye Hospital, Coimbatore, India
Panelist: Dr. Rilwan Ciroma Mohammed, Consultant, University of Abuja Teaching Hospital, Gwagalada, Abuja, Nigeria


[Muhammed] Good morning, everyone in Nigeria, and good afternoon in India. Welcome to the last webinar session for the year 2021 organized by Nigerian Pediatric Ophthalmology and Strabismus Society and supported by Cybersight. Our topic for today is superior oblique palsy, an illustrative guide to management with case examples by Dr. Sandra Ganesh at Aravind Eye Hospital, Coimbatore, in the state of Tamil Nadu in India. Dr. Sandra will give a short introduction on the etiology and assessment of superior oblique palsy. Following this, she will be showcasing seven to eight case examples including those with congenital and acquired onsets.

All of whom she had operated upon, detailing the pre operative assessments, indication for surgery, the types of surgeries done, and post operative outcomes. And then videos of the surgeries performed will also be shown to us. And at the end of the talk, the attendees will have a better insight on management protocols of cases with superior oblique palsy.

She will be speaking to us for about 45 minutes and then there will be 15 minutes for questions and answers. And then please you can post your questions during the course of the presentation.

Dr. Sandra Ganesh is from India, the land of Taj Mahal and Bollywood, the cricket capital of the world, and home to 1.3 billion people. That is roughly the population of Africa. Having worked for so long in a high volume tertiary eye care institute and referral center, Dr. Sandra has acquired vast clinical knowledge and surgical expertise in adult and pediatric cataracts and complex strabismus.

Ladies and gentlemen, I present to you our presenter for today, a dedicated pediatric ophthalmologist and surgeon by excellence and a passionate teacher, Dr. Sandra Ganesh.

[Sandra] I will be presenting on superior oblique palsy, an illustrative guide to management using case examples. Just to give you a brief overview, the superior oblique muscle is innervated by the fourth cranial nerve, or the trochlear nerve, which is a somatic motor nerve that innervates the superior oblique muscle. It intorts, infraducts, and abducts the globe.

The fourth cranial nerve has the longest intracranial course and it is the only nerve to exit through the brainstem dorsally. And it’s also a very thin nerve. This is very important to remember because it is very prone to head trauma. Superior oblique palsy is a frequent form of paralytic vertical strabismus and cranial nerve palsy. It can be either congenital or acquired. And it can present unilaterally or bilaterally.

Coming to the etiology. It can be either congenital, which can be due to hyperplasia of the nerve or a lax muscle or absent muscle. And acquired causes can be mainly just because of head trauma, which is around 44% of all cases. And oftentimes it is also because of microvasculopathy, including diabetes, hypertension, high cholesterol, or smoking. And inflammation in the region of the nerve and direct pressure because of nerves and tumors are very rare causes of superior oblique palsy.

Coming to the clinical presentation. If you see a patient who presents with a presumed superior oblique palsy, it’s very important to ask for photographs, old photographs. Because if it is present in all the photographs then it is a good indicator of a congenital onset of the disease. The patients usually present with head tilt, face turn, or chin depression. And they can present with vertical diplopia which can be constant or intermittent. And they can also complain of a tilt of the images and you can see the presence of vertical strabismus and sometimes the complaint may be mainly asthenopia or neck pain.
We definitely have to measure the face turn, the tilt, and the chin depression at the first visit. And we should document extraocular motility and see which muscles are overacting and underacting. And coming to the sensory evaluation, we need to note down the presence or absence of binocular vision and stereopsis, which usually will be present if the patient adopts anomalous head posture. With their head posture, they will have very good stereopsis. And the thing to remember is that in congenital superior oblique palsy, the vertical fusion amplitudes will be very large. Usually the vertical fusion amplitudes are only around three to four prism diopters. Whereas in a case with superior oblique palsy of congenital it can be around 12 to 16 prism diopters. Then we have to measure the deviation in the nine gazes.

As you can see in this picture, the patient is having a right superior oblique palsy and he has a right hypertropia. And the hyperopia increases in left gaze and it also increases on right tilt. You can see that on the contralateral tilt, it is not there. This is the anomalous head posture which the patient will adopt. And also then it is necessary to measure the amount of deviation with the help of prisms. The prisms are held base down for measuring the right hypertropia.

After noting down the prism values, then also we need to measure the subjective torsion and using a double Maddox, and objective torsion after dilation indirect and also fundus photography to document the amount of torsion.

What are the indications for surgery? In congenital cases, indications may be deterioration of binocular vision. That is as they grow older, the vertical fusion amplitudes may progressively become lesser. And so they might not be having intermittent diplopia. They may be unable to fuse for long even with the head posture. And another indication is severe torticollis because when a child presents with severe torticollis and that could result in progress of facial asymmetry. Because when the head tilt is there, in the ipsilateral side, the blood supply is less and that can lead to high atrophy in the dependent site.
And in acquired cases, the patients will be very symptomatic. And they will have diplopia, torsional diplopia, and they will be unable to walk or even look down. The treatment is aimed at resolving the diplopia, torticollis, and vertical, and the torsional deviations. And usually in acquired cases we wait for up to six to even 12 months after onset to operate further and after it is stable.

After we have decided that we have to operate, so what is the challenge? Because the treatment of superior oblique palsy is very complex and challenging, even to an ophthalmologist who has specialized in ocular motility.

Now I’ll be illustrating different types of superior oblique palsies with case examples. The first one is a 24-year-old male to presented to us with a sudden onset of binocular diplopia for the past two years, which was intermittent, and there has been no history of trauma. He has the best corrected visual acuity of 6/6 in either eye and anterior segment and fundus evaluation are within normal limits.

This is the patient, you can see that he has a right hypertropia in the nine gaze picture. And he has a measure around 20 prism diopters of R/L and that increases in the left gaze as you can see in the picture here. He has a right inferior oblique overaction here and that measures around 35 PD of R/L in that gaze. And he also has an underactive superior oblique, but the overaction of inferior oblique is more around +3. On ipsilateral field he’s measuring 40 PD R/L and in the other opposite field he’s fusing. Binocular vision is present with a tilt and there is a large visual fusion amplitudes.
His vertical fusion is around 12 and on fundus evaluation he didn’t have torsion. Diagnosis in this case is quite straightforward. It is a right superior oblique palsy, most probably congenital with decompensation. How much surgery should we do in this case? Here we see that the deviation in the primary position is around 20. When the deviation is 15 to 20 prism diopters, we can operate on a single muscle. And which muscle to operate? Whether you have to operate on the inferior oblique or the superior oblique because the deviation is more indicates of the inferior oblique. And also intraoperative forced duction test showed normal superior oblique tension and there was no laxity. In this case I performed a recession of the right inferior oblique to park’s point.

Following surgery, he’s left with a residual deviation of around eight prism diopters which increases in the direction of the inferior oblique. But since has very good fusion amplitudes, he’s able to fuse very well. His near deviation is only two, so it is okay to correct with only a single muscle. Here, if we operate on two muscles and that results in an overcorrection, then he will not be able to fuse because he will not have vertical fusion amplitudes in the opposite direction.

Coming to the second patient, is a 34-year-old gentleman who presented with deviation in his right eye since childhood. There has been a history of an old traffic accident in 2008 and he underwent plastic surgery for facial bone fractures. He did not have any anomalous head posture, but there was facial asymmetry, and also he had a huge hypertropia in his right eye of around 30 degrees.

You can see here, he has a very large right hypertropia and on prism cover test is measuring around 50 prism diopters. And the hypertropia is there in all the cases. And on the right tilt, the hypertropia is around 60 and on the left tilt, the right hypertropia is around 16. Here, as opposed to the first patient, this patient is having a very large hypertropia. Which is increasing to the left gaze and the right tilt.

Just keep in mind this case and I’ll discuss a few pearls because both are cases of congenital SO palsy. The second case, even though he had a history of road traffic accident, it has not caused an acquired palsy. The palsy was there even before and we had looked at all the photographs to confirm that. Congenital IV nerve palsies often present later in life due to decompensation from the gradual loss of fusion amplitudes that accompanies aging. And as I said before, these patients tend to display larger than normal vertical fusion amplitudes, around 10 to 15 prism diopters. The normal values are only around 1-3. They may present with a history of intermittent diplopia, especially when they are tired. And they may experience diplopia or asthenopia during prolonged reading. And it is beneficial always to examine old photographs or the patient’s driving license to assess for a longstanding head tilt or a torticollis. And facial asymmetry or hemifacial microsomia on the side of the preferred head tilt may also be noted.

The second patient is also congenital SO palsy. The forced action test showed a marked superior oblique tendon laxity. This is the second patient. You can see the forced action test being performed and this is a superonasal approach to tuck, you can see that the superior oblique tendon is really very long and lax. And in a normal patient you would not be having such a long superior oblique tendon. When the tendon is very long and lax, it is good to perform a superior oblique tuck. Around 4-8 millimeters of tuck can be done. Here I have done 6.5. That is done with a non-absorbable ethibond suture. And following that I come for again with the FDT before putting in a permanent knot. Initially I had put it as a slip knot, and finally I put it as a permanent knot. This is the superior oblique tuck being performed. And also because he has a very large angle I also combined it with the inferior oblique anterior transposition. In this patient we had operated on two muscles.

At the end of this you can see that one month post surgery, he has a vertical deviation of around 16 PD in the primary position. That increases in downgaze to a PD of 25 of vertical and also increases towards the left gaze. And in a few gaze positions, he’s able to fuse now. The thing is we can still, since he’s left with a residual, we can operate on the other eye, the inferior rectus, which will be the third muscle of choice. But the patient was actually happy with the outcome because he was able to fuse also and he said that he will come later for surgery if he feels that the residual deviation is significant.
The third muscle that we have to operate, in this case it would be the other eye, the left eye, inferior rectus recession. This is the inferior rectus. This muscle if we weaken, again, we can reduce the vertical deviation in that particular gaze.
Coming to the third patient, he’s a 50-year-old male who complained of deviation of his eyes for the past eight years. And he had double vision for the first eight years which was binocular. And all these complaints following head injury and he had fallen down unconscious around 10 years before.
This is his deviation, you can see that he has a left hypertropia and a left exotropia. And in the right gaze he is having a left inferior oblique overaction. And this is his fundus photograph where you can see that there is a very significant extorsion. Normally when you draw a line from the disc to the macula, it will be cutting the macula. But here you can see macula is very far down. Here we are using the prisms to neutralize the horizontal exotropia and the vertical deviation.
This is a case of an acquired superior oblique palsy. Since he has an exotropia, he also has a torsion, and he has vertical deviation. We decided on operating on the left eye, lateral rectus recession on adjustable suture for the exotropia combined with medialrectus dissection of around four. Inferior oblique anteropositioning and Harado Ito for the torsion. You can see that procedure here in the video.

This is the lateral rectus muscle which is being isolated. This is a limbal incision being performed and the 6.0 vicryl sutures are taken at the insertion. And I have also marked the point where the anterior fibers of the superior oblique need to be fixed. For this, a temporal approach is needed so superior oblique inserts temporarily as a fan. And the anterior ¼ of the fibers are responsible for the torsion. We need to split the anterior ⅓ and the posterior fibers and anterior ¼. And then take sutures, it is needed to do this with caution because the fibers are very thin and they can easily rupture. Now they are inserted around eight millimeters behind the insertion of the lateral rectus muscle. That is anterior rising the anterior fibers and that results in torsion and hence that is as a treatment for torsion.
Next, because of the huge vertical deviation and inferior oblique anteropositioning is also performed, this is the inferior oblique muscle which has been procured and sutures are being taken through the muscle. And we have to cut it as close to the insertion as possible. And after hooking the inferior rectus, the inferior oblique is anteroposed and it is sutured and fixated to the new insertion. That is the recession of the inferior oblique that has started weakening.

Finally, the lateral rectus muscle has been fixed on an adjustable suture because he had so many complaints, I wanted to put it on an adjustable slip knot because I wanted to go and see tomorrow whether he’s fusing and then fix the muscle at that position. This is the medial rectus muscle, four millimeters of medial rectus muscle is cut from its insertion and the muscle length is shortened. And again, it’s fixated to the original insertion. This is the end of the surgery.

Here you can see, if you remember the preop how big the extorsion was. Post operatively his extorsion is gone, in fact he had a small overcorrection and a mild intorsion. This is the immediate post operative photograph where you can see that the vertical deviation has fully been treated by the inferior oblique antropositioning. The exotropia is also not there now. Only in the downgaze he had some esophoria and he had a vertical deviation in downgaze. But the patient was happy with the outcome because in most of the binocular gaze positions he’s able to fuse.
Coming to the fourth patient. It’s a 21-year-old male patient who had an upward deviation of his left eye since early childhood. This was a very different case. We needed to use the chin up head posture to look with both eyes together. He had to maintain a chin up. He was using only in his downgaze. His unaided visual acuity was 6/6 in either eye and anterior segment and fundus examination was all within the normal limits.

You can see this is the way he presented. If he fixates with his right eye, his left eye went totally hyper. And he’s fixing with his left eye, that is the hypertropia of the right eye with a ptosis. He had a binocular single vision fusing with the chin up posture. As you can see here in this video, this is how he was fixing with the chin up. But the minute he looks up, there is a big upshoot of his left eye and in the downgaze positions he could fuse better. That is limited elevation of right eye in dextroelevation. That is left superior rectus overaction of +3 with near normal superior oblique function.
This particular patient we had a diagnosis dilemma. Because it was not falling into any particular picture. Whether the primary pathology’s in the left eye or in the right eye, we were not very sure at the initial presentation.

This is the prism cover test values. As you can see, in the primary with the chin up he could fuse very well. He had binocular vision and stereopsis like this. But in the first primary posture, his left eye will shoot up, all the up gaze position he had left superior rectus overaction and the vertical deviation was around 65-70 prisms in all of gaze positions. In primary position also the left L/R was around 55 and in the downgaze there is absolutely no vertical deviation. He only had the exotropia in downgaze. And on his ipsilateral tilt, it was 65, left hypertropia in the contralateral tilt it is only eight.
And this is a picture of the fundus showing extorsion in both eyes and the left eye being slightly more extorted than the right eye.

What was our differential diagnosis? Could it be just a right monocular elevation deficiency with a secondary overaction in his left eye? Or could it be a left superior oblique palsy with a left superior rectus contracture? Or could it be misinnervation?
In office we did a forced duction test in the left eye, and that revealed a left superior oblique tendon laxity with a mild tightness of left superior rectus and also mildly tight inferior rectus. All this we’re more in favor of a left superior oblique palsy. Then we decided to operate on the left eye because the deviations were also more on the left eye. And intraoperatively, the forced duction test showed a very lax superior oblique tendon. Here is the superior rectus muscle which is being hooked. We decided to recess the superior rectus muscle also. This is the superior oblique muscle which is being hooked here. And you can see how long and lax the tendon is. This is, again, a feature of congenital superior oblique palsy. The tendon is really long and lax. As Dr. Kekunnaya had said, the namaste sign that Indians hold their hands together and we did a tuck there.

And here now the superior rectus is also being recessed by around eight millimeters because of the overaction of the superior rectus muscle in our case. And the lateral rectus and now you can see that the inferior oblique muscle here, I decided to do an anterior nasal transposition of the inferior oblique. Usually we do the temporal recession, but here I am bringing it under the inferior rectus and fixing the muscle nasally. Because this will serve to the depressed eye that is having a more stronger depression action when you do an anteronasal transposition and followed by the lateral rectus recession. Here we have operated on four muscles, but since two are oblique muscles there is no danger of anterior segment ischemia. The recti muscles are the lateral rectus and the superior rectus muscles. These are the muscles we had operated on four muscles for this patient.

And this is the post operative outcome. Here, this is the post operative nine gaze picture. The pre operating, you can see gaze positions all having the upshoot in the left eye. After the superior rectus recession, the upshoot is totally gone. And primary position also he could better fuse without the chin up posture, and the depression also is okay. This was the values of prism cover test. Mainly in the primary position and the downgaze position, the patient is able to fuse easier. In upgaze he still had the vertical diplopia. He no longer had to maintain the chin up posture to fuse, and he had good fusion in most of the gaze positions, except in extreme upgaze and downgaze. And also following the left superior rectus recession, his upshoot on the left eye has disappeared. This was the outcome.

Some cases you may have a diagnostic dilemma. When you have such cases it is always better to rely on the forced duction test findings and also intraoperatively you can explore and see the muscles and then decide on the course of surgery that you have to take. But the consent from the patient is very important. You have to define all these terminologies in the consent form and then do accordingly.

Coming to the fifth patient. It’s a 30-year-old male. Again, he had a history of road traffic accident. This road traffic accident is a major cause of these acquired superior oblique palsies, especially if there is a loss of consciousness with severe injuries. He had a head injury with a subarachnoid hemorrhage about 10 months prior. He underwent a conservative neurological management and recovered completely. He noticed double vision which was mainly in downgaze, for the past four months. Since he worked in a textile dyeing industry, he could not resume work because of diplopia and hence he had a loss of livelihood and that was the major concern here.

Here you can see that in the primary position, this is his nine gaze photograph, he’s quite well-aligned and he has only two prisms of esophoria in the primary gaze. And on the left gaze, he had four prisms R/L. Whereas in the right gaze, he has four prisms L/R. This is the alternating hypertropia on gaze positions. In the downgaze, he’s having 18 prisms of esotropia. 18 of esotropia with the same vertical in the downgaze. And on the left tilt, he had 10 prisms of L/R and in right tilt he had six prisms of R/L.
In upgaze positions, all upgaze positions, he could fuse well and he had no diplopia. That’s why he was having the chin down posture. But with the chin down posture, it is not possible to work or look down when he’s working with textiles nor is it possible to walk downstairs. That’s also a major concern. This, if you can see, it is a V pattern esotropia, with alternating hypertropia. These are features of bilateral acquired SO palsy. This is still bilateral SO palsy case.

This is his fundus photograph. You can see that he’s having torsion in both eyes. Both eyes there is extorsion and in the double Maddox rod. My double Maddox rod is a very useful tool to measure the subject to torsion. We have to use two Maddox rods, two red or one red and one white, over either eye and use a penlight torch to illuminate. And ask the patient to rotate the Maddox rod and then you can measure the subject to torsion.

What are his main concerns? Main concerns are the chin depressed posture, the torsion, and the diplopia in downgaze, he had all these problems. I think one of the most difficult cases to treat is this esotropia in downgaze along with the torsion. Because if he wanted to eat, the mind vertical in primary position, that is not going to treat his symptoms. Unless you are going to address the torsion, the patient will not be able to fuse with any prism that you are giving. Any patient who has anything more than 10 degrees of torsion, you have to address it surgically. Unless you treat the torsion, we cannot treat the double vision. He will not be able to fuse. Torsion and diplopia, there is no other way of making them fuse apart from doing the surgery, that is the Harada Ito procedure. Alternating hypertropia, V pattern esotropia in downgaze, and significant torsion. The diagnosis is acquired bilateral SO palsy with a V pattern esotropia.

How do you treat esotropia in downgaze? For esotropia in downgaze, bilateral inferior rectus recession is a good option because inferior recti or the rectus. Once you recess the inferior rectus in downgaze, they do not adduct that well and so the esotropia is treated. And here we had decided on a ⅓ tendon with temporal transposition. The recession cannot be, may or may not be combined with a small temporal transposition for the esotropia. We did not do a larger degree of temporal transposition because if you do a temporal transposition, that will worsen the torsion that he’s having now. We did it very small in ⅓ tendon transposition. Sometimes it is not necessary to do that also. And then we also decided to operate on the left superior oblique and had a Harado Ito procedure that will address the torsion.

This has to be done very symmetrically because he didn’t have any vertical deviation in the primary. Not much vertical deviation, very small vertical deviation he had. We should not induce any new deviations in the primary position. This is the inferior rectus muscle. You can see that the muscle is being recessed here. And this is the four millimeters of recession. This is the original insertion and here you can see that there is a small temporal transposition which has been done. This is the new insertion of inferior rectus muscle. And here this is the superior oblique, the Harada Ito, the anterior fibers which have been hooked here. And that’s fixed close to the lateral rectus about eight millimeters behind the incision of lateral rectus.

Post operatively, this is his picture. In primary he still had the same vertical deviation, but maybe it could have been a better idea to recess the inferior rectus a little more on one side. On the right side, about five and left around the four I could have done, thinking back. But since it was very symmetrical the vertical deviation has remained the same. And in the downgaze, from 18 prisms the esophoria it has come to six prisms only. Now he’s very not that symptomatic in the downgaze diplopia.

This is the fundus picture. The single eye or the right eye procedure had corrected the bilateral extorsion. How is that? Because whenever the patient sees with the paralytic eye, he will actually see the torsion in both eyes. Even by operating on the one eye, in both eyes the torsion has gone. And there is no subjected torsion also in the double Maddox. And he had an improved field of binocularity except extreme downgaze. So he could go back to work and he did not have chin depression also.

Coming to the sixth patient. She’s a 38-year-old lady who had a history of road traffic accident. It was a head injury with a fracture of the right maxillary sinus and lateral orbital wall around one and a half year earlier. She noticed double vision in downgaze, mainly on climbing down the stairs since then. And she had to tilt her head to see clearly with the chin down posture.

This is her picture. In primary gaze, she had a small exophoria. And here it is mainly only a left hypertropia. The right eye it is only in the left side. It is a left mild superior oblique paralysis. And you can see that the inferior oblique is also not that overacting here. In fact it is not overacting at all. And in the downgaze, also, there is a very mild underation of the superior oblique muscle and at -1 you could see it. There is normal ductions. On the downgaze there is a hypertropia of around 12 prisms in primary and 16 prisms in downgaze. This was the reason why she could not fuse and she was having vertical diplopia. And on the ipsilateral tilt it was 18 prisms L/R and on the contralateral right tilt it is four prisms L/R.

Again, she had an acquired left superior oblique palsy. There is no deviation in upgaze. The more deviation is there in primary position and downgaze. And she had a moderate hypertropia in primary gaze, as you could see from the nine gaze picture, a moderate hypertropia in the primary gaze which increases on downgaze. The good part is, she did not have torsion on double Maddox rod testing. This patient it is not necessary that all acquired cases should have torsion, but you definitely have to rule out. It is much more common in acquired cases than in congenital cases. Congenital cases they do not usually present with torsion. Probably because there is some degree of the brain has probably got adjusted to that position of the eyeball. Congenital cases don’t usually present with subject to torsion. Acquired cases, very oftentimes do.

There is no torsion on the double Maddox rod testing. Here, the main concern was the hypertropia which is increasing in the downgaze. Because of this variation between primary and down, we did a Scott’s procedure that is on the right eye inferior rectus, a resect/recess procedure.
What is this Scott’s procedure? When you have an incompetence like a primary value which is less than at a gaze position, you can actually resect the muscle and then recess it so that will reduce the incompetence. It can also be done for a near distance disparity on the medial rectus muscle, also it can be done. Or on a superior lateral rectus palsy also if there is a near distance disparity you can do a Scott’s procedure.

Post operatively, here we had done a two millimeter resect followed by four millimeter recession of the right inferior rectus. She’s orthophoric in primary and near gaze and she still has only around six prisms of L/R in downgaze. In the primary she is orthophoric and there is no diplopia. She was happy with the outcome but she had a minimal vertical in extreme downgaze position.

Coming to the seventh patient. He’s a 49-year-old male patient. He had double vision for the past four years following a road traffic accident. Uncorrected visual acuity he has monocular visual acuity of 6/6. He had an MRI done in 2018 and that showed some post traumatic gliosis in the left basi frontal cortex, subtle thinning and atrophy of the left superior oblique muscle.

This is the patient. And the Worth Four Dot testing he had diplopia, both for near and distance. And also he had 15 degrees of extorsion of his left eye. On his nine gaze measurements, you can see there is a left L/R of around 10 prism diopters in primary. That increases in the right gaze. As you can see from the pictures, also, he has hypertropia which increases towards the right gaze. The superior oblique is underacting, inferior oblique is overacting. Downgaze also there is a large vertical. The vertical deviation is 10 prisms in primary and 25 prisms of L/R in downgaze. And on the head tilt to the left it is L/R of 20. Head tilt to the right the L/R is six. And also he had 15 degrees of extorsion in his left eye. He had a lot of problems because he, again, was an electrician and he could not look at the wires, he was not able to look towards his side gaze at all. He was using, mainly he had a huge face turn and he was fusing with using his left gaze positions.

Here, again, because there was a huge difference between the vertical between primary and downgaze, initially I thought that I could do a Scott’s procedure on his right inferior rectus to reduce the vertical deviation between the primary and downgaze. We were not very sure about the extorsion, subjectively the Maddox rod testing, he couldn’t cooperate well because of the huge vertical component. We thought that we would address this first.

The right eye inferior rectus resection at 2.5 with a recession of four millimeters of the Scott’s procedure was done and a local anesthesia in his right eye. Following this procedure, this was the immediate post operative finding. It had come down to eight and 14. Initially it was 10 and 25.
This is one month later. One month later, he continued to have a left hypertropia of eight in primary, downgaze is 12. The incompetence has come down. Earlier it was 10 and 25 and now it is eight and 12, but still, there is a significant hypertropia in the primary position. And that increased now, if you could see this more in these gaze positions, where it becomes 25. And on the head tilt it is 20, left head tilt. The right head tilt it was only two. Now he complained of torsion. Because the medius had come closer together, he could appreciate the torsion better and he had a torsion of 10 degrees in his left eye.
Still he was not happy, this patient. His head posture was better than before, so his chin down posture had come down a bit, but still he couldn’t fuse very well. As you can see here, the inferior oblique muscle is overacting.

This is the fundus picture. You can see in the left eye there is extorsion, this is the right normal eye. And left eye that is an extorsion, not as much as previous patients whom I showed, that is not a large extorsion of 13. This patient is having only around 10 degrees of extorsion.
Here, now we decided to operate on the left inferior oblique, a recession, because of the inferior oblique overaction, along with the Harada Ito procedure for the torsion and a local anesthesia. This is a video of the surgery. Here you can see. The thing to remember is that Harada Ito is a very strong procedure. When we are tightening the amount of extorsion, how to tighten it? If you put it very close to the lateral rectus, it will correct more. Whereas if you put it about, and don’t pull it down so much you can correct several degrees of extorsion also.

Here this is the inferior oblique anteropositioning is just being done. And now I’m hooking the superior rectus and you can see the superior oblique fibers, this is the temporal approach. The anterior ¼ of the fibers are hooked and the ethibond suture is tight. And now I am fixing it a little about, I’m not taking it way down until the lateral rectus, a little about. Because the amount of extorsion that needs to be corrected is only 10. And then we are doing it as you can put a slip knot and see that you evaluate the torsion the next day and then you can judge. Or else you can do on table direct after dilating the eye and you can see how much extorsion is being corrected and then you can tighten it also. Those are the ways of doing it.

At the end of this here, you can see that now he’s fusing very well in primary position. And the vertical deviation is existing only in the downgaze positions now. So there are now, out of nine gaze, five gaze positions he is able to fuse.

And also this is the post operative. See here, this is the pre operative extorsion in his left eye. This is the post operative picture where you can see that the extorsion has also gone corrected. It is very easy to overcorrect extorsion if we pull down the Harada Ito muscle fibers very tightly, then that can overcorrect the extorsion. That also, we do not want. Initially, probably, it is better to put it on adjustable suture knot and then see and titrate and then decide upon the tightness.

I think we have discussed many different cases of superior oblique palsy including a lot of congenital and acquired presentations. The few things that I would like to conclude and say is that a single muscle surgery alone may be required if the hypertropia is small. If the primary PD is around 15, less than 15, you can operate only on single muscle. Either you decide which muscle based on where the deviation is high. If the deviation is more towards the inferior oblique, then you operate on the inferior oblique. If it is more towards superior oblique and the superior oblique is very lax, then you can do a superior oblique tuck. Those two will be the initial muscles of choice.

Ipsilateral inferior oblique weakening, contralateral inferior rectus weakening is also an option if the deviation is mainly downgaze. Superior oblique tucking to be done only if the forced duction test shows laxity. Because if you tighten a normal muscle it can do certain iatrogenic down syndrome so you don’t want to create a tight muscle.

Harada Ito is to be operated if there is torsion. Fibrosis of the superior rectus can certain limitation of depression in abduction. In long-standing acquired cases of primary because of continued hypertropia that can cause fibrosis of superior rectus. That results instead of competence with hypertropia in more direction, primary and abduction. If that is so, and if superior rectus is found tight on surgery, then you can do a superior rectus recession.

We prefer to operate on two muscles if the primary angle is more than 15-20 prism diopters. Ipsilateral two oblique musical surgery is an effective procedure for moderate to large angle deviations in congenital superior oblique palsy. In adult position, if you do ipsilateral two oblique musicals, then you can avoid general anesthesia because you are doing surgery in one eye only and it can be performed in a local block also. Intraoperative, every time you do a tuck on the superior oblique muscle, always confirm by doing the FDT and see whether you’re not tightening it too much, do the intraoperative FDT and then do the final tuck.
If there is associated horizontal strabismus, which is quite frequent, around 50-60% of patients there can be associated horizontal strabismus, both in congenital and acquired palsy. If the surgery on the horizontal recti has to be done only if the deviations are significant, more than 8-15 prism diopters. Because the less severe horizontal deviations can resolve by operating on the cyclovertical muscles alone. Thank you.

[Mohammed] Thank you very much, Dr. Sandra for the beautiful presentations.

[Sandra] The questions, yes. There is a question on if you have a three-year-old child presenting with the left 45 prism diopters hypertropia, facial asymmetry from birth, would you operate right now? In this particular child, if we are having a very large hypertropia and we are sure of the measurements, and if the child is having significant torticollis because of the hypertropia, I think since the angle is so high, it is safe to operate. Provided the operating surgeon has good experience on operating cases of superior oblique palsy and has operated on a number of patients in the older age groups earlier on. I think it is quite safe to operate on this child provided that general anesthesia fitness and other things are there.

Initially they can explore and see the superior oblique tendon, if it is quite lax then they can combine a tuck with an oblique recession. And still there may be some amount of hypertropia which is left behind and that can be operated later on. That will help the child to fuse and may avoid amblyopia also.
All these cases when you’re operating on small children it is very important to rule out refractive error and amblyopia and if such a case scenario is there it is better to treat with occlusion therapy and best corrective glasses
The second question, it seems you prefer an anterior position of inferior oblique, why? Because anterior positioning of inferior oblique, if the hypertropia is quite large, then I prefer to do anterior positioning because it gives a stronger depression action. In one particular case I did an anterior nasal transposition also because it depends on the amount of hypertropia in primary position. Recession may not be able to correct that much of hypertropia in the primary position. So that is the reason.

There is a third question. I have a patient with marked underaction of the left superior oblique. After posterior tenotomy of bilateral superior oblique for bilateral SO overaction. What would you advise for iatrogenic superior oblique palsy? Is it a full tenotomy? If it is posterior, usually a posterior tenotomy of superior oblique will not result in a iatrogenic superior oblique palsy. The posterior tenectomy is quite a safe procedure and it’s mainly to address the gaze pattern. And it will result in collapse of gaze pattern.

But if there has been such a scenario then for iatrogenic SO palsy, I would treat as any other case of SO palsy. We need to see how much of the torsion is there, and whether that is vertical in the primary position. Just see if there is underaction, I think we need not operate. But if the patient is having symptoms, if there is a vertical division in primary position, then we can do the nine gaze evaluation, and then decide on operating on the inferior oblique. Or if there is significant torsion then we need to address that. Usually the iatrogenic superior oblique palsy are falling full anatomy of the superior oblique muscle.
[Adio] Superior oblique palsy is something that a lot of people have issues with in trying to understand it. And Dr. Sandra has broken it down to bite size. And we’re able to understand it much better. Thank you very much for being with us.

[Sandra] Superior oblique palsy I think when we train our trainees, superior oblique would be the last muscle they usually operate on. Compared to that, the inferior oblique is a very forgiving muscle because it does not create, when you do the recession we can do myectomy, or we can do a recession. But still there is not much problem in inferior oblique even if you go wrong. But superior oblique, both assessment and what decision to operate matters a lot because we need to first diagnose the superior oblique palsy. And also rule out multiple cranial known palsies, especially in case of head trauma or other etiology, diabetes. You can have a fourth and a sixth nerve combined together. We need to rule out multiple cranial nerve pathologies also. And Park’s test usually works only for single muscle palsies, it doesn’t work well for multiple cranial nerves. We need to remember that. And a very important thing is the documentation and measuring in all the nine gazes and then we have to document the presence or absence of stereopsis.

Because most of these patients are patients who are fusing well, so that is what we need to remember. Whether it’s congenital or acquired superior oblique palsies, they usually are able to fuse with their head posture. These patients will have good binocular vision and diplopia with their anomalous head posture. Since that is there, we should try to improve their binocular field following this surgical correction. But if we are creating a new torsion or a new vertical deviation, or we are reversing the vertical deviation, the problems usually arise because the patients will not be able to have fusion. Even in those cases which they were fusing before. That is what we need to remember and that is why very meticulous planning is important in the case of superior oblique palsies.

Inferior rectus is when we do the prism cover test in the nine gaze. And we are having a vertical deviation which is more in the downgaze, which is more towards the inferior rectus. Because the superior oblique and inferior rectus are yoke muscles we can have superior oblique underaction combined with the inferior rectus overaction. There are some acquired cases where the inferior rectus will be overacting, but the ipsilateral inferior oblique may not be overacting. When we are doing the nine gaze position measurements, we will get more of a vertical deviation in downgaze.
In acquired cases, since superior oblique duct is not an ideal option because the tendon will not be lax in a case of acquired SO palsy. The other option will be to recess the inferior rectus muscle. And so that will help to reduce the vertical deviation in downgaze. We can do that fixed procedure on an adjustable suture. That will help you reduce the vertical deviation in downgaze.

The other condition that I was talking about was the Scott’s procedure where the primary position deviation vertical is there and there is more vertical in downgaze. That is an incompetence which is more in downgaze, the vertical is increasing. For such cases, for the inferior rectus instead of pure recession, you can do a small resection followed by recession. With will reduce the incompetence between the primary and the downgaze measurements. That is another case where inferior rectus can be used to attack superior oblique palsies.

Harada Ito unilaterally cause and used to torsionally fix? Harada Ito is always done unilaterally. It is because in acquired SO palsies, when the torsion is more in one eye, we have to evaluate how much of torsion in there in either eye and see whether it is a masked bilateral superior oblique palsy or if it is a unilateral superior oblique palsy. If the torsion is more in one eye, then we can do that Harada Ito procedure on that eye alone. And it will not create any new torsion. It will reduce the torsion that is already there. We are doing the Harada Ito procedure in a patient who is having extorsion in order to correct the extorsion.
The problem comes when the extorsion is very mild. When it is around only five degrees of extrusion, Harada Ito may not be a choice because then it can overcorrect the patient. Harada Ito is a choice when the torsion is about 10-15 degrees of extorsion. Then you will not create an overcorrection in that eye. If there is a case where both eyes are significantly extorted, then we can do Harada Ito bilaterally in that patient.

[Muhammad] In the absence of any other questions, I would like to thank Dr. Sandra Ganesh for taking time out of her very busy schedule to give us this talk on superior oblique palsy. We’d also like to thank all of the participants for making up time to listen. And then, of course, the leadership of the Nigerian Pediatric Ophthalmology and Strabismus Society for organizing this and Cybersight for providing the platform.

[Sandra] Thank you, thank you, Dr. Adio, thank you Dr. Rilwan, and Cybersight for connecting all of us together. Thank you.


December 05, 2021

Last Updated: October 31, 2022

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