Photodocumentation of Non-Surgical Treatment of Strabismus

LN is an adorable 2 year-old who I first saw last November after his mom had attended a seminar I gave about visual processing.  She came up to me during our lunch break and asked if we could chat about her son.  As an occupational therapist she found it difficult comprehend why the pediatric ophthalmologists to whom she’d been taking her son did not share her concerns.  When I saw LN for the first time had a large angle left eye esotropia with a preference for fixating with the right eye, evident in the picture here.  He had undergone periods of occluding one eye and then the other to counteract amblyopia, but all this seemed to do was to make his nystagmus worse, and was therefore discontinued.  (There is no history of strabismus surgery or other binocular treatment, and I have elaborated on his history below in the “Comments”  section.)  Mother realized it was time to get a therapeutic opinion.

There is a good reason why LN turns his head to the left, because he has a left lateral rectus paresis.  Unable to even get the left eye to the midline, looking outward with that eye seemed impossible.  However LN still managed to use the left eye well enough to prevent amblyopia from developing.  This is because of a special condition known as cross-fixation.

Cross-fixating occurs in esotropia, where the right eye is used to look toward stimuli in the left visual field, and the left eye is used to look toward stimuli in the right visual field.  LN was only able to abduct the right eye slightly past the midline, and the left eye not at all. The way we counteract cross-fixation is to apply binasal occlusion to a pair of spectacle lenses, in this instance with no prescriptive power.  We do this by placing a strip of translucent tape of the inner half of the lens – from the center of the child’s pupil to the nasal corner of the lens.  Now the left field is inaccessible to the right eye, and the right field is inaccessible to the left eye.

With the binasal tapes in place, and mother restraining LN’s head from behind, he is now able to move the left eye outward past the midline, and no longer has nystagmoid movement on lateral gaze.

The same holds true when LN looks rightward, able to abduct his right eye outward as mother lightly restrains his head from turning in that direction.

What is most encouraging is that LN is now able to exhibit periods of eyes aligned with this binasal occlusion in place with his head in the straight-ahead position.  As long as he continues to develop increasingly longer periods of alignment, there is no need to consider any further surgery, which is all the pediatric ophthalmologists had offered to LN’s parents.

On his most recent visit to me, LN’s mother told me that he loves playing games on her iPad.  We’ve therefore moved toward using the iPad as one of his vision therapy activities, and he is beginning to be able to hold his head straight some of the time without any lenses in place.  At other times, his mother has him working on the iPad with red/green filters taped over his binasal spectacles, and a red or green filter on the iPad screen.  So far, so good!

– Leonard J. Press, O.D., FCOVD, FAAO

33 thoughts on “Photodocumentation of Non-Surgical Treatment of Strabismus

  1. Sorry, I don’t follow — how did the nasal occlusion correct a paretic muscle? Was the LR paretic from surgical recession (unlikely if the surgery was for ET, though maybe this is a consecutive ET?). The pictures don’t look like Duane syndrome (no fissure changes); isolated CN VI palsies occur at this age relatively rarely.

    As you know, cross fixation in infantile esotropes does not occur due to muscle paresis. So maybe either the “cross fixation” or “paresis” terminology is inappropriate in this particular child.

    What was the etiology of his “end point nystagmus” in your opinion? Hemi-field occlusion isn’t a typical nystagmus treatment. I am not experienced in binasal occlusion therapy, and request your edification. My understanding was that this is used for “peripheral vision awareness”. Shouldn’t covering one eye (in either field of gaze) aggravate nystagmus as well as reduce fusional capability?

    • Thanks for your comments, Dr. Ticho. No excuse, but I uploaded the photos late last night without any notes on LN and confused some of his history. I’ve gone back in and updated it to clarify that he did not have prior strabismus surgery. My primary purpose in sharing the case was to show the potential role for non-surgical intervention, beyond what had been previously suggested, which had been limited to alternating occlusion. I’ll address that further below. In other cases we’ve used binasal occlusion post-surgically as part of a therapeutic program to aid fusion. A good reference that summarizes the apporach was written by Tassinari. Here’s the link:

      Click to access 1-1%20Tassinari.pdf

      With LN’s file in front of me, here is his elaborated history:

      1. Diagnosed with tuberous sclerosis prior to birth.

      2. Cardiac rhabdomyomas noted and patient treated with the antiarrhythmic Amiodarone.

      3. Full-term birth and no ocular abnormalities noted post-natally.

      4. At 3 months mother began to notice esotropia of both eyes on downgaze coupled with a pendular nystagmus. LN was referred by his pediatrician to the ophthalmologist who noted “questionable mild nystagmus both eyes with variable esotropia” and recommended no treatment and 2 month follow up. Within one month both the horizontal nystagmus and esotropia lessened considerably.

      5. At 4 months mother began to notice vertical nystagmus, principally in upgaze, which spread in short order to all fields of gaze. The ophthalmology report of exam at 8 months indicates some concern that the nystagmus may have been caused by use of Amiodarone. The report documents vertical nystagmus in all fields of gaze with esotropia absent. No treatment was recommended, and follow up advised in 4 months.

      6. At 11 months LN experienced a seizure and was put on Keppra. Mother reported that as the dose was gradually increased, the nystagmus concomitantly decreased. Coincident with the nystagmus decreasing, the esotropia began to increase and LN adopted a head turn. [To my knowledge this wasn’t nystagmus blockage syndrome, as acquired or increased esotropia is usually associated with horizontal rather than vertical strabismus, although point #4 is noteworthy for the brief period of horizontal nystagmus and ET interaction].

      7. At 16 months there was a pediatric neuro-ophthalmology consult. The presence of two tubers in the parieto-occipitial region seen on an MRI was noted. At that time ocular motilities are notated as full with alt ET, R possibly more esotropic than L. Occasional upbeat oscillations were noted. Recommendation was made for starting monocular occlusion with the following comment: “This is important in strabismus prevention. Full strabismus prevention may not be completely practical or possible given that he has tubers in regions of the brain that control vision”. It was recommended that he be monitored every six months.

      8. I initially evaluated LN at 19 months of age. Mother recapitulated the history above. EEGs have been normal. I found OKN responses to be absent horizontally N/T and T/N but present vertically in both directions. Constant esotropia was present with cross-fixation. Abduction was limited but present with the R eye but LN was unable to ABD L eye past midline. LN had habitual head turn to L to compensate for absence of abduction OS. There was no abduction nystagmus, end point nystagmus, or latent nystagmus noted, and pupillary responses were normal.

      9. I applied binasal tapes to lenses and demonstrated activities to be done, with Luke’s head restrained. We refer to this as “abduction calisthenics”. The idea of using binasal (hemi-nasal field sector) occlusion to discourage cross fixation, and to use abduction calisthenics to improve LR ABD function is outlined by Dr. Ralph Garzia of UMSL here:

      10. LN returned one month later and his mother and I both noted decreased esotropia in primary gaze. Without his glasses on she was noticing that LN brought objects very close to his face (he has no ametropia). I took that as a healthy sign that he was beginning to develop a binocular centration point.

      11. LN returned a month later, now at 22 months of age. ET was now intermittent, and mild end point nystagmus was noted on ABD. ABD was now greater to the L for the L eye (apx. 45 deg outward from midline)than to the R for R eye (apx. 20 deg outward from midline). I advised his mother to work ABD calisthenics in both directions to try and achieve symmetry. We also added a red filter for use as an MFBF procedure. (Reference on MFBF is: Cohen AH. Monocular fixation in a binocular field. J Am Optom Assoc 1981 Oct;52(10):801-6)

      12. One month later LN exhibited a range of apx. 70 degree ABD OS and 60 degree ABD OD. In primary gaze he remained a variable angle alt ET with brief periods of alignment, more so with binasals in place. There is a residual habitual head turn to the L in primary gaze. Retinoscopy continued to be plano OD/OS with near retinoscopy showing normal near accommodative responses. In addition to standard ABD calisthenics, I encouraged mother to continue rotating LN’s head in Doll’s Eye fashion to develop reflex ABD movements.

      12. I most recently saw LN on 5/31/11, now at age 26 months. OKN is now sluggishly developing horizontally. ABD is now full to either side. Nystagmus is absent. Most recent MRI shows the two parieto-occipitial tubers unchanged (see #7 above). We will continue to work on sensorimotor fusion, peripheral procedures, increased time in wearing binasals. I also always leave the option open of strabismus surgery if LN regresses instead of progresses in fusion, though given his neuro-ophthalmic sequelae above this has to be weighed carefully in terms of cost:benefit ratio. I monitor him every 3 months at this juncture.

    • I’d like to ask Ben Ticho what is his thoughts are on the cause of cross fixation in infantile esotropia?
      I’ve seen some that will break down with repeated dolls eye maneuver, and others that have not.
      Regarding end point nystagmus, Tychsen’s and Brodsky’s work in this area suggests limitation of movement and Nasal to temporal motion processing seem to be the initial factors.

      • Well, I’m a little out of my depth on this one, particularly given the changing nature of his nystagmus. To summarize: Tuberous sclerosis with seizures and parieto-occipital hamartomas. Infantile pendular evolving to upgaze-induced upbeating nystagmus with apparent resolution by age 19 months, and subsequent end-gaze horizontal nystagmus. Infantile-onset constant ET (possibly V-pattern, as noted more in downgaze) with associated cross-fixation and variably reduced abduction OU, becoming intermittent over a 3-month period (from 19 to 22 months). Treatments employed = encouraging abduction to either side (passively / actively using binasal occlusion, “calisthenics” while fixing the head position, and repeated doll’s head movements).

        I appreciate the Garzia reference, but am still uncertain about the utility of binasal occlusion in treating cross-fixation. (In essential or infantile esotropia, cross-fixation is not entirely undesirable, as it discourages development of a fixation preference / strabismic amblyopia.) These patients do not typically have abduction deficits per se — as Dr. Baxstrom states, good abduction is usually easily demonstrated (as we do to show the parents and residents that the problem is not lateral rectus weakness). I expected Dr Press to explain that binasal occlusion reduces excessive medial rectus stimulation (presumably by Sherrington’s law). But maybe that’s not the right explanation?

        I also don’t understand how binocular fusion was apparently achieved, given the evolution of a constant ET to an intermittent one. It doesn’t seem that dissociative treatments like monocular (nasal) occlusion or monocular red glass tinting would promote binocularity. There was apparently no accommodative component (the glasses pictured appear to be plano OU?). I need more educating on this….

      • You’re doing fine, Ben, and I’ll piggyback on some of Curt’s comments. He posed some nice questions, the answers to which will also help clarify my understanding on your thoughts about etiologies.

        Regarding terminology, I was taught as Curt that paralysis is total inaction of the muscle and paresis is partial paralysis, i.e. there is still some range of motion in the normal field of action, but is limited.

        My primary consideration for binasal occlusion in this case was that in preventing cross fixation of the right eye, the left eye is forced to abduct to maintain fixation temporally. Habitually these patients when following a target to the left, will follow with the esotropic right eye (cross fixating) and rotate their head to the left to continue following with the right eye. The left eye never has to abduct, particularly when the child is free to rotate his had leftward unrestrictedly. (And same holds true for opposite eye opposite side.) That is the reason we have the parent restrain the head which forces abduction by:
        1) eliminating cross-viewing with the ET eye due to the nasal tape
        2) eliminating substitution of head movement for eye movement

        Our models are a bit different because we seem to accord more possibility of repetitive sensory-motor movement expanding range of motion. While divergence is more difficulty to develop than convergence, it isn’t impossible. Parenthetically, the same holds true with vertical vergence ranges.

    • In this case the child definitely had limited abduction at the time I first saw him. The habitual head turn to the left is also consistent with this, and when I occluded the left eye and mother restrained his head from behind, he was initially unable to ABD past the midline. Assuming that prior reports lacking observations of a head turn, and evidence of full motilities were accurate, we should be able to reverse the ABD deficit by ocular calisthenics. To my way of thinking this should be much different than a physical therapy/orthopedic synergy. If there are signs of variability, work on increasing range of motion.

      Regarding the utility of binasal occlusion in treating cross-fixation, I realize that cross fixation is desirable in preventing strabismic amblyopia. But we are also looking at procedures that encourage binocular alignment and fusion. In the convention application of binasals, one disrupts the central suppression of the esotropic eye. In cross-fixation the esotropic eye actually becomes the centrally fixating eye for viewing the contralateral field and is not suppressed. Binasal occlusion is disruptive of the habitual pattern of viewing the contralateral field with the esotropic eye. The idea is to restore viewing of the temporal field with the ipsilateral eye on each side.

      In this case there was no hyperopia present. Both the ophthalmologists and I are looking for any evidence of hyperopia or an accommodative esotropia, but to date none is evident.

      • Okay, I’m getting closer. The binasal occlusion is an anti-suppressive treatment. (Whether or not cross-fixation necessarily means there is temporal field suppression more than nasal field suppression, I don’t know — when he alternates suppression, wouldn’t each eye’s temporal field be also alternatingly activated?)

        But even if this type of monocular sensory change was taking place, how does it
        a) correct a paresis (muscle weakness caused by nerve damage = partial paralysis)? (Again, I think part of the problem might be terminology. I don’t doubt that the child didn’t abduct well on basic versions, but was the limited abduction really, really paresis? Did you test abduction after while prolonged patching the opposite eye?)

        and b) promote binocular fusion? Even if anti-temporal field suppression therapy were occurring, there doesn’t seem to be a binocular stimulus strong enough to overcome human’s limited divergence abilities to overcome infantile esotropia (which usually has large amplitudes, although in the photos provided, it looks pretty small, hardly present at all on the top picture).

        Forgive my denseness, I’m still not understanding. But this is all useful for me — I appreciate your efforts to educate a VT neophyte.

      • I’d like to ask for some clarification from Ben.
        1-What do you believe is the cause of the initial cross fixation pattern?
        2-Regarding abduction deficit, when are you usually observing that you have full abduction ability in the infantile eT cases?
        3-Can we clarify paresis vs. palsy? I’ve usually considered palsy a complete paresis. Most infantile eT cases are partial paresis cases, atleast early on. This might be why you are uncertain about the recovery of paresis with a binasal.
        4-We have other issues that have not been discussed on the abduction deficit and binasals. Modifying contracture and atrophy secondary to the limited abduction and/or cross fixation pattern. And lastly, Guyton last year did his Bielschowsky Lecture on the last adaptation, the roles of vergence tonus and muscle length adaptation. These seem like likely areas of improvement by eliminating the cross fixation pattern.
        5-Lastly, I’d be more afraid of monocular occlusion to cause amblyopia/disruption of binocular vision development versus a situation of free alternation that is set up with binasal occlusion.

      • Sorry to beat this paresis thing into the ground, but calling cross-fixation and infantile esotropia a “partial paresis” implies (denotes is probably the more appropriate term) a partial CN VI palsy, something which, to my (limited) knowledge, has not been demonstrated for this entity. I’m sure given all the EMG studies Henry Metz and others did during the 60s and 70s, they would have found something so basic. Knowing how frequently infantile ETs go XT over time (even without surgery!), it seems unlikely that a partial LR palsy would be the primary etiology. The only infants in whom I can’t demonstrate good / full abduction (most commonly with simple doll’s head maneuver) have Duane syndrome, or, occasionally, CN VI palsies from head trauma or space-occupying lesions.

        I am emphatically not an expert on EOM electrophysiology, so can only parrot what others have said about the etiology of infantile esotropia and cross fixation. It makes intuitive sense that there is somehow “increased convergent neural input” to the medial recti, but my understanding of all the simian research on this is limited. (Again, increased “tone” to the MRs doesn’t mean there has to be reduced innervation or paresis of the LR.)

        To say that this is not a LR paresis doesn’t mean that binasal occlusion might not accomplish something useful clinically. I’ve never tried it; maybe it does change muscle tone, as Dr. Baxstrom surmises. Having operated on many 80-PD infantile esotropes, I have been surprised that medial rectus contracture is actually absent when performing forced ductions. But there it is.

        I am intrigued by the idea that binasal occlusion may cause the MR tone to decrease by encouraging divergence. Are there electrophysiologic studies of this? If this hypothesis were supported, it would obviate the theoretic need for a LR paresis, which I still maintain is unlikely. (The problem I envision with my hypothesis is that binasal occlusion may not produce divergence at all but rather just a version movement, with esotropia still evident in the nonabducting eye. In this case the MR tone might not be decreased after all.)

      • To offer an additional thought regarding a possible mechanism for why binasal occlusion was more than antisuppression or peripheral awareness training is to look at the research of Taub, et al in the area of Constraint-induced movement therapy with stroke patients. Here is the study: Constraint-Induced Movement Therapy: a new family of techniques with broad application to physical rehabilitation–a clinical review.
        I think there could be a case made for use of binasal occlusion as an example of “forced abduction” ie constraint-induced movement, as the patch interfers with the preferred motor patten (crossed fixation) and helps to facilitate the neural development of improved abduction, divergence and binocular fusion for this type of esotropia.

  2. Well done, so do you know the time of onset? With the lateral abduction deficit, I’d guess more likely early on. The LN was likely related to lack of development of N-temporal motion processing, often seen in those that don’t abduct well. Especially in infantile eT. Would be nice to look at motion processing both pursuits and okn from N-T. Compare R vs. L. We’ve been adding use of Liberman’s eyeport with some of these kiddos, alternating R and L fixation while converging and diverging. As well as some of David Cook’s activities using an MIT and polaroid/RG glasses. Good luck, Curt

  3. Congratulations on your success in this exciting case. I’ll be curious to know if the left lateral rectus paresis dissipates with time and with use.

    It would also be nice to have some relative measure of the neuro-muscular gain, and whether this changes over time. For example, would a phoria measure be different in this patient with the left eye fixating versus the right eye fixating? I suspect it would be higher with OS fixating. Is cover testing asymmetric with neutralizing prism held OD vs OS?

    Thanks for sharing!
    Warm regards,


    • Thanks for the comments, Samantha. I have been using Hirschberg reflexes as a guide rather than neutralizing prisms because it’s always challenging just to get LN to fixate in primary gaze, to control his head turn, and to document his abduction range. There are no prism measurements or even angle estimations in any of his ophthalmologic or neuro-ophthalmologic reports, so I can’t give you any clues from that either. But you point is well-taken and something we’ll continue to try to obtain in the future.

  4. The mystery of abduction deficit and it’s relationship with cross fixation pattern is often confusing. I believe there is a reason for this.
    1-Most infants don’t freely look laterally until after 3 months, where the cross fixation pattern is then observed, and that I believe the early abduction deficit is the initial reason for the infantile eT cases.
    2-Most infants with infantile eT are not see by eye doctors until well after 6 months
    3-The abduction deficit can decrease overtime, mostly gone by 9 months, but can persist. In reality, I believe there are many different types of infantile eT cases, mostly depending upon the duration of the abduction deficit and sensory/motor adaptations occuring secondarily to it.
    4-Thus many of these patients are thought to not have an abduction deficit, as only the infantile eT , with a common crossfixation pattern is observed later on.(This is not much different than an initial accom. eT becoming later a case of partial accom. or non-accom eT.)
    5-I believe the key for these patients is to: A-use binasals to break cross fixation pattern and promote lateral tracking(this should promote ipsi eye to lead to ipsi visual field. B-Work on abduction deficit using pursuits, saccades, OKN and VOR to use ocular motor subsystem transfer to maximize gains. C-This should lead to the decrease in the vergence angle, and move the infant toward fusion and the recovery of binocularity. D-Lastly, emphasis can be placed upon improving Nasal to Temporal motion processing during the use of binasals to promote the recovery of stereopsis. This is supported by Tychsen’s thoughts on motion processing being one of the key adaptations that need to be solved for improving stereo. See his motion/okn chapter in Simons book : Visual Development, normal and abnormal, 1993.

  5. I read the Tassinari article on binasal occlusion, which was very useful in improving my understanding. I couldn’t help noticing his conclusion, however:

    “A rationale for [binasal occlusion’s] effectiveness has been offered that is based on existing literature but is not assumed to be proven. The relative paucity of literature concerning binasal occlusion has probably contributed to its poor acceptance by some. Clinical success on a case by case basis has encouraged others to use it regularly. Additional case reports, clinical trials, and controlled research would serve to substantiate the use of binasal occlusion…”

    I know much of what we do clinically has not been substantiated by prospective, randomized, controlled, masked clinical trials. But this seems like something that could be readily tested. It’s such an inexpensive technique, it seems worth finding out whether it truly works (and how, if possible).

  6. Ben- Thanks for your further input and insights. Language sometimes can muddy the water when discussing such topics as we are. You continue to use palsy, which to me seems very less likely as well. You’ve suggested a partial paresis is also not likely. So maybe the term you’re looking for is pseudoparesis, in which the infant will not abduct cortically, but you can drive it atleast to some degree with the dolls eye.

    This however is difficult for me to completely accept as many I’ve seen earlier on(4-6 mo) do not budge after 4-5 alternate head rotations. I will get some of these to move with 5 and sometimes up to 10 full rotations and observing the post rotary nystagmus begin to move the eye laterally. I would suggest that the paresis(pseudo or otherwise) is dynamic and on a continuum vs. an all or nothing phenomenon. It does change over time. And the infant at 9 months can easily be left with an established esotropia, and if not seen earlier, an abduction deficit(cortical or subcortical) could easily have led to this in the first place.

    Tychsen in his chapter on infantile esotropia from Clinical Strabismus Mgmt-principles and surgical techniques p.130 states, “Frequently, marked degrees of abduction deficit are not fully overcome by rotation”. Again, the key here is when they are seen, not if they have it or not. Von noorden in his book on binocular vision suggests they, “exhibit apparent defective abduction and excessive adduction or both”.

    So if an infant has inf eT and abduction deficit, it makes common sense to try to drive eom laterally to counterbalance the MR. Most OMD’s I know here prefer to monocularly occlude to try to break it. But again, if you look at vonNoorden’s book, he states that “Interfering with fusion(monocular occlude) you may precipitate a manifest deviation”. So if one considers these points, why would one ever try to use monocular occlusion and risk the onset of a strabismus and even amblyopia? The use of a binasal makes much more sense as it provides the opportunity(and we implore our parents to use this binasal for therapy!) to provide frequent alternate fixation without cross fixation.

    This further supports the literature from Tychsen who demonstrates poor OKN and pursuits in infantile eT. A binasal provides a heavy emphasis on alternation of Nasal to temporal tracking, especially when one considers it versus a monocular occlusion. A cross fixation pattern does not provide the stimulus to help recover or establish nasal to temporal tracking.

    The last consideration is your comments on the “normalcy” of abduction which is based purely on subcortical eom by the dolls eye. If we really look at the problem, the cortically driven motion processing and pursuits are the core of the problem and can more easily be addressed with a binasal. In day to day life, the infant still acts like they have a LR paresis, atleast cortically. So suggesting they are ok because you can drive it subcortically does not influence their ability in day to day scanning. If it wasn’t a cortical processing problem, then it makes no sense that an infant would switch to the contra eye when passing midline while following a target. Here the infant cannot track N to temporal and thus the contra eye picks up fixation without the binasal because the contra eye pursues it in a Temporal to nasal direction more readily.

    Binasal and selective occlusion is not used only by Optometry, but also by OMD. Stefan Rethy of Germany, whom passed away several years ago and Sarniquet-Badoche from France have published multiple articles on its use. Rethy published a nice overview titled, Mistake of strabology, really early treatment of infants neglected, in Congenital disorders of ocular motility, ed. by A. Casanera deMolina, 1989. I corresponded with Stefan for many years, he regularly presented his thoughts on occlusion(and on Donders’ as a component) at the ESA and APPOS meetings.

  7. I’m going to defer to Curt’s comments, Ben. He has had alot of experience with these case types, and I don’t have much to add beyond his points. I was heavily influenced at the outset of my career by some of the French and German work on sector occlusion.

    You made a good point about studies, and I realize it seems on the surface interventions like these should be easy to study, but it rarely is as easy as it seems. Working with binasals requires alot of cooperation on the part of the child as well as the parent to obtain sufficient use of the Rx, and in controlling head posture so that the child has sufficient exposure to 1) abduction calisthenics and 2) eliminating cross-fixation. This is defeated by the child looking over the glasses, or refusing to have his head restrained and rotates into the contralateral field to view with the opposite eye.

    Although I always welcome controlled studies, I tend to side with von Noorden when he wrote: “If we can accept without a controlled study that aspirin is an effective analgesic and that cataract extraction improves vision, we should also be able to accept that occlusion therapy for amblyopia is effective.” I’d broaden that to include any intervention for strabismus or amblyopia.


  8. I like “pseudoparesis” which allows the observed reluctance to abduct without implying the inability to do so. Dr. Baxstrom’s comments about cortical vs. subcortical eye movement initiation are intriguing, and the fixation switch likely has a cortical processing origin (makes sense). I don’t claim great knowledge on the neurobiology of eye movements (bluntly, “I don’t know”).

    The comments against monocular occlusion probably don’t apply to cross fixators. Kids who alternate fixation shouldn’t need to be patched from an amblyopia perspective. If one further accepts that they rarely have a true abduction deficit, than patching to encourage abduction isn’t indicated to “strengthen” a “pseudoparetic” muscle.

    Most cross fixators have large, non-fusable angles, so monocular occlusion is unlikely to be interrupting fusion — unless you’re referring to ARC-type peripheral fusion, I suppose. We could have another discussion about ARC, but suffice it to say that I’d rather have NRC (in other words, correct the ET and go for bifoveal function)!

    Alternate monocular patching shouldn’t be too much different than binasal occlusion in terms of the goal of breaking abduction reluctance — and possibly much more practical. I haven’t prescribed this, but to the extent that one wants to encourage abduction in cross fixators, it would seem to do at least some of the same things (without the parental head restraint).

    The issue of cross fixation timing is intriguing. I agree with Dr. Baxstrom that parents don’t bring kids in for ET evaluations early, especially in the first 3-4 months. I think cross fixators actually get referred pretty early, as parents are concerned that their child’s eyes “don’t move” which isn’t the usual infant alignment variability that they assume kids “grow out of”. So I’m unconvinced that there’s a lot of undiagnosed cross fixation going on in the first months — maybe, but Steve Archer’s infant studies didn’t show that, so the burden of proof goes the other way. I also am suspicious that cross fixation “goes away”. Once a kid has given up on binocularity and is happily alternating, why would it spontaneously resolve?

    Regarding Dr. Cross’ comments on not needing controlled studies for common practice, I would have agreed with him in the past, until the PEDIG started making hash out what we thought we knew. Two hours a day of patching is good, but obviously 4 is better, and all day must be even better, right? Atropine is fine, but surely it won’t be as good as patching, especially for 20/200 amblyopes. Older kids don’t usually respond to patching. Near work activity is important in amblyopia treatment. That’s a lot of “common knowledge” that has been (at least partially) debunked. Same thing with CITT, which suggested that pencil pushups don’t work. Yes, these studies have flaws — they might even be “wrong”, but they do expose the danger in relying too much on “it worked for my teachers, it works for me, so it doesn’t really need to be studied.” In the case of binasal occlusion, the apparent fact that it is so difficult for parents to perform (how long / often do you have to do the head restraint thing?) makes demonstrating effectiveness even more desirable.

    Anyhow, I’m going to get some binasal occluders and play around with them in the office. If Dr. Press doesn’t mind my gentle skepticism, I’ve subscribed to this blog — as I get older, broadening my brain is key to preventing stagnancy, ossification, and irrelevance. I’ll try not to be a pest….

    • I like “pseudoparesis” as well. I question whether alternate monocular occlusion can accomplish the same thing as binasal occlusion. Although total occlusion of the cross-fixating eye forces the pseudoparetic eye to abduct, it doesn’t allow any room for fusion. So from a practical standpoint, there is an advantage to:
      1) the parent not having to keep up a schedule to remember to switch the patch back and forth between the two eyes and
      2) leaving room for bifoveal fixation

      In both instances the parent has to restrain the child’s head, because they tend to rotate to compensate for poor abduction. I’ll jump down to your end query in which you asked how long/often parents have to do the head restraint thing. I only apply the regimen when I have a parent who I feel can comply with the protocol. In this case mom is an OT and very comfortable doing therapeutic activities with little ones (however, as we know, it’s always easier to work with someone else’s kids than your own!). The key here is quality time, more than the number of hours, but I suggest a minimum of 30-60 minutes per day. These are young kids with whom a parent is (hopefully) interacting in activities. The idea is to break it up into chunks of time whether watching a favorite TV show, while having a favorite snack with food approaching from the side, or playing with a favorite toy – the idea being to associate it with reward than than being punitive or restrictive. Having said that, I recognize it’s not an easy thing to do.

      I love what you wrote about the PEDIG study. In the Archives of Ophthalmology article in 2005 there was a great editorial which summed it up. They wrote: “As physicians we pride ourselves in our use of scientific method to give the best care to our patients. Yet many of our daily decisions reveal us more as apprentices than scientists. We choose a particular treatment not because a clinical trial determined that it worked better, but because that is the way our mentors did it.”

      I’m sure you catch the irony that this was in 2005, when for all those years VT-ODs were taking it on the chin for being “non-scientific” and functioning as apprentices. That levels the playing field.

      Here’s a pertinent comment from the NEI background on that 2005 study:
      “Most eye care practitioners believe that there is an age beyond which attempting to treat amblyopia is futile. It is generally held that the response to treatment is best when it is instituted at an early age and is poor when attempted after 8 years of age.”

      So aside from the number of hours required for patching, there is the upper age limit for treatment. Now here’s where there’s an important difference. You wrote: “PEDIG started making hash out what we thought we knew”. But the “we” of Optometry knew that long before. If you look at our literature we’ve been presenting data for many years that plasticity extends well beyond age 8 (see Birnbaum et al 1977 J of American Academy of Optometry & Physiological Optics), and that all day occlusion wasn’t necessary. Part of the problem seems to be what we are students of your literature to a much greater extent than vice-versa. We’ll talk more later! In the interim, thank you for subscribing to the blog, and the wonderful tenor of your comments.

  9. Ben- Thanks for your thoughts on cross fixation and pseudoparesis. So I believe what I’m hearing is these infantile eT cases are done to promote recovery of the pseudoparesis. I would still suggest that a binasal is far better than alternate monoc occlusion for this and for the recovery of fusion. There are multiple reasons, here are some:
    1-EOM chapters suggest that the lateral rectus leads in abduction, with the MR getting secondary input with another connection. Why this system is programmed we may assume to be oriented toward cortical issues, but if you use a binasal you’re promoting the LR to lead in abduction, and you are teaching alternation of the two LR to lead as well.
    2-These infantile eT cases show nasal to temporal motion processing that is maldeveloped. A binasal would again promote Nasal to temporal, but also that ability to more N to T motion processing between the two eyes.
    3-A binasal actually decreases the size of the fusional fields between the two eyes, emphasizing more localization with each eye. I believe one of the effects of this is for the abducting eye to retake the position of directing localization cortically. Less emphasis on fusion. One of the common things we will do is once the patient can reset the abducting eye to lead localization, the binasal can then be reduced, allowing recovery of fusion.
    4-You’ve stated these infantile eT are large angles, but I only find them large when well off midline. The binasal eliminates the need for active suppression to take place, and thus the size of the angle can also reduce. As we know, if one cannot suppress, generally one must increase the angle to eliminate the confusion/diplopia. Thus decreasing the need to actively suppress also supports the recovery of binocularity in these cases.

    Most of all I’d like to thank you for considering these new thoughts into your treatment regimens. I believe you will be satisfied with further learning and many of these patients will recover.

  10. I forgot to comment on one other part that keeps getting caught up in the discussion of these patients. Len’s patient had a unilateral condition in which therapy included the need to hold the childs head stable to promote abduction, otherwise the child would turn his head. With infantile eT, I have never had to hold an infants eyes as the ability to abduct is equally poor, and they never seem to rotate their head.

    Instead, we primarily have parents support therapy by playing games while they are changing diapers, eating, etc. alternating the target(face, food, bottle, etc.) from R to L side promoting free alternation between the R and L eyes while visually localizing and improving the pseudoparesis.

    Thus it is really much easier in my mind where we can work with the infant all walking hours, whereas a patch must be continued to be rotated, etc. Curt

    • Just to clarify, Curt, my patient’s lateral gaze restriction wasn’t unilateral – abduction was difficult for both OD and OS. There was asymmetry, so we had her spend more time doing ABD calisthenics to the side that was more restricted, and now she is doing 50-50.

      There’s one point you made that I’m not quite following. When you work with cases of what we’ll call pseudoparesis, when you have parents supporting the therapy by alternating the target as you note above, why wouldn’t the child simply continue to alternate eyes? What are you doing specifically that reduces the pseudoparesis?

  11. Len,
    Thanks for clarifying this, I thought I recalled mention of it primarily being one side. In the infantile eT cases, all but a couple have been fairly equal in the pseudoparesis. I really don’t see too much head turning as we put the target to localize well off to the side and they begin to decrease the abduction deficit.

    In the case where we have binasals in place, the patients generally do begin to alternate with no pseudoparesis. Thus they are recovering the abduction eye as the primary eye in localizing laterally. I’ve had 4-5 cases now that did not improve in 3 months or so. In these cases we referred the patients to a cranial osteopathic physician. This is where it becomes more hypothetical in my thinking as it is well outside the normal box of thinking. the DO suggests it comes down the cn 6 involvement by the petrosphenoidal (also known as Grubers) ligament. The suggestion here is it partially obstructs normal neurosignals of CN 6. In these cases, I have not seen the dolls eye or repeated rotation with prn affecting the eom, it still wouldnt’ go beyond midline. These are the “toughest” cases. He adjusts the palate from inside the mouth and this supposedly loosens the relationship between the nerve and the ligament, and I’ve had spontaneous release seen the next day. There is no other cranial nerve I know of that has a ligament laying over the top of it. It also I believe can explain the variations in types of pseudoparesis from those that sponaneously recover to those that resist recovery.

    The other part of the question I think is why might they begin to lead with the lateral eye and not crossfixate anymore. Here I think it is still a wide open question. But I think you’ve got increased use of the decussation fibers from nasal retina leading toward localization thus a different cortical mapping perhaps? But also Tychsen makes a good foundation that the development of N to T motion parallels steropsis development, thus the N-T tracking from binasals perhaps leads to fusion/stereopsis? I have more questions myself than answers, hopefully over time we’ll better understand this population.

    The activiites we provide are similar to the tx activities we use for tbi/cva patients. Thus trackign is broken into pursuit, saccades, motion(okn/cloth usually) and also head tracking in opposite so dolls eye looking at his parents. Mom’s face, large targets, etc….

  12. Mr. Len Press,

    When I was a child I had to have my eye glasses taped to correct amblyopia in my right eye. Now as an adult I still have residual R eye crossing inward, that is more prevalent when I’m tired (esotropia). I also have problems with stereo vision, my brain only wants to use my L eye when given binoculars for example. I’ve gone to see an eye Dr. to see if they could offer me any kind of therapy or exercises to improve my condition and they basically laughed at me and said that I need nothing and I’m not a candidate for surgery. What method of glass taping would help me to better focus my right eye centrally and remove the esotropia and help the stereo vision?


  13. Len,

    Thanks for the quick reply and the resources. I found a Dr. close to me and schedule an appointment. Hopefully they will be more helpful than my last eye Dr.

    Thanks again.

  14. Dear Dr. Press, on behalf of myself and some other interested VT mom’s I would like to know how this boy is doing 5 years later. He must be around 7 years old right now. Perhaps his parent would agree on sharing an update with us? Has VT fully corrected his esotropia?

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