This is for a dear friend. 

This is a good review explaining the subtle difference between Central Fusion Disruption Versus Horror Fusionis.

Dr David Hunter, a former colleague at Harvard, is a world’s leading expert in this diagnosis. 

There is nothing in the literature to suggest going gluten free will help with the above types of double vision, but this below link was interesting. 

https://www.verywellhealth.com/gluten-ataxia-symptoms-562398

Sandra Lora Cremers, MD, FACS 

Diplopia in Patients with Anomalous Binocular Function

This includes diplopia from anomalous retinal correspondence (ARC), horror fusionis, and central fusion disruption. Diplopia secondary to ARC is one of the most feared forms of diplopia after strabismus surgery, as it can be both unexpected and refractory to treatment, leaving patients permanently diplopic despite an anatomically successful result. ARC develops in patients with longstanding, generally large-angle strabismus as a sensory adaptation that functions as a crude form of binocularity. In ARC, the brain configures a pseudo-fovea in the retinal area of the strabismic eye that corresponds with the object of regard during binocular viewing (the pseudofovea exists only during binocular viewing, disappearing during monocular viewing; patients with ARC do not have eccentric fixation). When surgery alters the relative position of the strabismic eye, the pseudo-fovea no longer corresponds with the object of regard, and diplopia results. For example, an esotropic patient with ARC will experience crossed diplopia (simulating exotropia), despite an orthophoric result. These patients have little or no potential for bifoveal fusion, but neither have they learned to suppress the image in the strabismic eye. The result is intractable diplopia that does not respond to prism or exercises; even more distressing is that, in some cases, the pseudofovea disappears, and reversing the surgery will not eliminate the diplopic image. In our experience, most of these patients remain functional despite the constant diplopia, as they are readily able to discern which image is the “real” image perceived by the fixating eye and which image is the “false” image produced by the misperception of the nonfixating eye. In the weeks and months following surgery, they learn to ignore (but never to suppress) the second image. There are rare exceptions when the only recourse is to permanently occlude one eye. Related forms of postoperative diplopia are central fusion disruption and horror fusionis. While the terms are often used synonymously, some authors distinguish the two terms: horror fusionis (literally, “fear of fusion”), a term coined by Bielschowsky, is the active avoidance of bifoveal stimulation.10

 This tends to occur in patients with infantile-onset strabismus. In contrast, central fusion disruption is an acquired phenomenon where bifoveal fusion is not possible. 

This tends to occur after closed head trauma, brainstem hemorrhage, and 

related injuries.11 A defining characteristic of horror fusionis is observed in 

the synoptophore as a “speed effect,” in which an image swept across the retina of the nonfixating eye with constant velocity appears to speed up, then slow to a stop, then “jump over” the fixation target in the fixating eye.12 This may also be observed in patients with central fusion disruption.

Injuries and illnesses causing central fusion disruption are often associated with acquired strabismus at the time the injury occurs; it is only after anatomically successful or nearly successful strabismus surgery that the fusion deficit is discovered, and the frustration of unexpected postoperative diplopia results. We have found that, while in some cases patients will eventually learn to fuse, in most patients there is no relief of diplopia, despite correction of the horizontal, vertical, and torsional disparity with a combination of surgery and prisms. In contrast to patients with diplopia from ARC, it can be difficult for patients with diplopia from central fusion disruption to decide which image is perceived by the fixating eye and which is perceived by the misaligned fellow eye. For this reason, many authorities advise that it is best to leave the strabismus unoperated in these patients out of concern that moving the two images closer together will make it harder for patients to make that determination. We have found, however, that when the strabismus is corrected early, patients prefer to have the images as close together as possible. Once the location of the second image has remained stable for many years, patients will become uncomfortable if the image shifts to a new location, whether through spontaneous drift or additional surgery.

Another rare form of diplopia we have observed in patients with anomalous binocular function can occur in amblyopic patients who lose vision in their sound eye and, either as a consequence or in association with the injury or disease that causes vision loss, they also develop strabismus. In these patients, the forced switch in fixation from the sound eye to the amblyopic eye lifts the suppression of the amblyopic eye but without initiating suppression of the sound eye.

References:

1. 

ABSTRACT

Diplopia is a disappointing and, at times, unanticipated consequence of what might otherwise be considered anatomically successful strabismus surgery. In this study, we review the existing literature regarding diplopia after strabismus surgery in the context of the senior author’s experience. We divide postoperative diplopia types into cases that occur in the setting of normal binocular vision (or “normal” suppression) vs. cases that are the consequence of rare or anomalous sensorial adaptations. We then discuss how to identify patients at greatest risk based on history and preoperative testing, and we offer strategies for managing these sometimes-challenging cases.

Diplopia has a negative effect on both the functional and psychosocial aspects of life.1 

Strabismus surgery is often performed to eliminate diplopia, as well as to restore normal appearance, improve binocular vision, expand the field of binocular single vision, and/or reduce a compensatory head posture. Unfortunately, the desired result is not always achieved, and when preoperative diplopia is present, incomplete improvement in symptoms might be anticipated. In some cases, however, existing diplopia may be exacerbated, or new diplopia induced, by strabismus surgery. In this review, we will describe the different types of postoperative diplopia, how to identify patients at risk for developing this complication, and measures that can be taken to alleviate or eliminate symptoms in affected patients. 

CLASSIFICATION AND MANIFESTATIONS

Postoperative diplopia can be classified into two broad categories: (1) diplopia in patients with normal binocular function or “normal” suppression, including surgical overcorrection and torsional diplopia; and (2) diplopia in patients with anomalous binocular function, including anomalous retinal correspondence, horror fusionis, and central fusion disruption.

Diplopia in Patients with Normal Binocular Function or Suppression

Overcorrection is one of the commonly encountered reasons for postoperative diplopia after strabismus surgery.^{2–4 In horizontal strabismus surgery, diplopia is commonly encountered when exotropic patients become esotropic.5,6 Diplopia is less common (but by no means rare) after surgical overcorrection for esotropia. Diplopia is also quite bothersome for patients when a preoperative hypertropia is overcorrected to become a hypotropia. Even very small overcorrections may be poorly tolerated.}

An important secondary complication of diplopia after strabismus surgery overcorrection is the potentially permanent loss of binocular vision. Children who are overcorrected will readily acquire the ability to suppress. In such cases, intervention to eliminate the overcorrection (through prisms, botulinum toxin intervention, or additional surgery) should be performed promptly to restore binocularity before suppression becomes irreversible.

Torsional diplopia can be a particularly disabling complication in patients who had normal binocular function prior to strabismus surgery. The new torsional disparity generally has to be quite severe to create symptoms, as most normal individuals have a robust torsional fusion capacity. On average, normal subjects tested with large-field stimuli can generate eight degrees of cyclovergence, and they can further generate an additional eight degrees of sensory cyclofusion. Thus, up to 16 degrees of surgically induced cyclodisparity can generally be overcome with normal cyclofusional adaptations.^{7 When the amount of induced torsion approaches or exceeds this amount, torsional diplopia results. When torsional disparity is the source of diplopia, it is necessary to perform torsional surgery; however, it is not necessary to perform extreme procedures in an effort to reduce torsional disparity to zero. If the postoperative difference is reduced to within the range of cyclofusional and sensory adaptation, the patient’s torsional diplopia should be eliminated.}

TREATMENT

For patients with normal binocular function or suppression, postoperative diplopia can usually be treated successfully by reversing the direction of overcorrection; that is, to convert a sequential esotropia back to an exotropia (or orthotropia), or to restore a sequential right hypotropia back to a right hypertropia (or orthotropia). This can be achieved with prisms, botulinum toxin injections, or additional surgery. For patients with anomalous binocular function, treatment can be considerably more difficult. If the diplopia is in response to an overcorrection, the first step would be the same as that with individuals with normal binocular function or suppression—to attempt to restore the preoperative alignment. We have seen cases branded as ARC diplopia that turned out to have small overcorrections; these patients responded nicely to additional surgery. The most challenging cases are patients who continue to experience diplopia despite attaining the desired postoperative result. In many if not most of these cases, assurance and the passage of time can be powerful remedies, but for patients who are incapacitated and demand action, more drastic measures are necessary. These include complete reversal of the previous surgery (though, in such cases, even attempting to restore a 30 PD esotropia may not eliminate the diplopia if the patient ends up with an esotropia of, say, 28 PD or 33 PD, or if the pseudofovea is no longer present.) Since reversal of the previous surgery may not eliminate diplopia and will once again create the problems with social interactions that led the patient to pursue surgery in the first place, this should be reserved only for the most severely symptomatic patients. Another option is to attempt to occlude or blur the non-dominant eye using overcorrection with glasses, contact lenses, or adhesive tape. This can work well in patients with dragged fovea-diplopia syndrome, where a small patch of centrally located fogging tape can mask the disparate foveal image while not interfering with peripheral fusion. Extreme intentional anisometropia by placement of an intentionally under- or over-powered intraocular lenses has also been proposed as a treatment for intractable diplopia in strabismus patients,20 but in our 20+ years of experience caring for patients with complex strabismus, we have not yet offered that option.21 In many patients, optical fogging of any degree is not adequate, as they are not able to suppress the second image and it impinges on the “real” image; when that occurs, patients may need to be treated with a black occlusive patch over the non-dominant eye; a black, occlusive contact lens; or even a black intraocular lens.15,16

For patients who appear to have some risk for ARC diplopia, we have found that the use of the “short-tag noose” adjustable suture approach can be reassuring.17 The advantage of this technique is that it allows for suture adjustment to be performed a full week after surgery. This gives the patient time to decide whether the postoperative diplopia they are experiencing, if any, is going to be tolerable; if not, the surgery can be reversed before the muscles have healed into place. We have, in our experience, had one patient who asked to have the surgery reversed: this was a 35-year-old attorney with a lifelong history of a 30 PD exotropia, who had an exotropia of 0 on postoperative day 3 but was experiencing intense diplopia. The procedure was reversed in the office in several steps, and the diplopia was not eliminated but became acceptable to the patient when the exotropia angle had been increased back up to 12 prism diopters, where it remained with 10 years of follow-up. For patients with central fusion disruption who have diplopia despite very small residual postoperative strabismus angles, we recommend using prism to try to bring the angle down to zero in primary gaze. In rare cases, fusion will recover, sometimes after months have elapsed. In many, reassurance that there is nothing more to be done and that with time they will learn to suppress is sufficient. When central fusion disruption is acquired later in life, unfortunately, despite excellent postoperative alignment, complete occlusion of one eye remains the only acceptable option for some patients.

REFERENCES

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2.

Central Fusion Disruption Is Not Horror Fusionis

Reddy and colleagues1 describe 2 interesting case studies illustrating what has been referred to as central fusion disruption. In their introduction,

they make a not uncommon “mixed metaphor” error of diagnoses, confusing central fusion disruption with horror fusionis.

Horror fusionis is indeed a term coined by Biel- schowsky2 but it refers to a specific clinical syndrome wherein patients actively avoid bifoveal fixation. It is an active or dynamic process that, fortunately, is clinically rare. In 30 years of clinical practice, we have seen only 1 patient with this syndrome. In resident instruction we teach it as an active process of unknown origin (a few theories are offered) characterized by an affected pa- tient actively rejecting bifoveal stimulation by whatever clinical maneuver or instrumentation that is used. There is an active avoidance of sensory fusion. Supposedly, mo- tor fusional amplitudes may be measured but our exrience is so limited that we have never been able to con- firm that this is the case.

Central fusion disruption, or acquired motor fusion deficiency, was first described in German literature in 19353 but not by Bielschowsky. We teach this as a pas- sive process wherein affected patients have no or almost no motor fusional amplitudes but their sensory fusional apparatus is functionally intact. When bifoveal fixation is achieved, stable single vision arises. Unfortunately, patients with this condition cannot make the fine motor fusional movements required to maintain bifoveal fixa- tion throughout their everyday life, so they are sympto- matic, with intractable but variable diplopia and an in- ability to maintain stable single vision for any useful period of time. As is the experience of most who deal with ocu- lomotility disorders, most of these patients present with closed head injuries of various sorts in the expected age group for motor vehicle accidents and after vertebrobasi- lar distribution cerebrovascular accidents in older persons.

We would like to thank Reddy et al for yet another pos- sible etiology of central fusion disruption, not horror fu- sionis. The 2 uncommon syndromes are quite different.

Wayne W. Bixenman, MD

Author Affiliation: Department of Ophthalmology, Uni- versity of Arizona, Tucson, Arizona.

Correspondence: Dr Bixenman, 1500 N Wilmot Rd, Ste 180, Tucson, AZ 85712 (wwbix@aol.com).

Financial Disclosure: None reported.

1. Reddy SK, Salgado CM, Hunter DG. Central fusion disruption following ir- radiation of neoplasms in the pineal region. Arch Ophthalmol. 2009;127(3): 337-338.

2. BielschowskyA.LecturesonMotorAnomalies.Hanover,NH:DartmouthCol- lege Publications; 1956.

3. Jaensch PA. Fusionstorungen nach Gehirnerschutterung. Klin Monatsbl Augenheilkd. 1935;94:470.

In reply

Dr Bixenman states that central fusion disruption and hor-

ror fusionis are 2 distinct clinical syndromes that are often

confused; however, the literature is anything but definitive

on the topic. Classic texts such as Duke-Elder’s System of

Ophthalmology1 and Burian-von Noorden’s Binocular

Vision and Ocular Motility2(p146) make no such distinc-

tion. In Rosenbaum and Santiago’s more recently pub-

The mutually exclusive definitions proposed by Bixen- man have not, to our knowledge, been articulated in the lit- erature but on careful review of the original descriptions we agree that there are advantages to differentiating between the 2 terms. Central fusion disruption can be con- sidered an acquired phenomenon in which bifoveal fusion is not possible. Horror fusionis (literally, fear of fusion) can be considered the active avoidance of bifoveal stimula- tion, as first stated by Bielschowsky.7 Although Biel- schowsky’s cases of horror fusionis had congenital strabis- mus, there is no reason to believe that the phenomenon cannot be observed in patients with central fusion disrup- tion. Horror fusionis is associated with characteristic syn- optophore speed effects in which an image swept across the retina of the nonfixing eye with constant velocity appears to speed up, then slow to a stop, then jump over the fixation target in the fixating eye.4 Pratt-Johnson and Tillson6 have described a similar “bobbing” phenomenon in patients with central fusion disruption.

Sashank K. Reddy, MD, PhD Cristian M. Salgado, MD David G. Hunter, MD, PhD

Author Affiliations: Department of Health Sciences and Technology, Massachusetts Institute of Technology, Bos- ton (Dr Reddy); Harvard Medical School, Boston, Mas- sachusetts (Dr Salgado); and Department of Ophthal- mology, Harvard Medical School, Children’s Hospital Boston, Boston, Massachusetts (Dr Hunter). Correspondence: Dr Hunter, Department of Ophthal- mology, Harvard Medical School, Children’s Hospital Bos- ton, 300 Longwood Ave, Boston, MA 02115 (david.hunter @childrens.harvard.edu).

Financial Disclosure: None reported.

 lished authoritative textbook on strabismus, Clinical Stra- 3

1. 2.

3.

4.

5.

6. 7.

Duke-Elder S. Aetiology of squint. In: Duke-Elder S, ed. System of Ophthal- mology. Vol VI. St Louis, MO: CV Mosby Co; 1976:243.

Von Noorden GK. Burian-von Noorden’s Binocular Vision and Ocular Motility: Theory and Management of Strabismus. 3rd ed. St Louis, MO: CV Mosby Co; 1985. KraftSP.Selectedexotropiaentitiesandprinciplesofmanagement.In:Rosen- baum AL, Santiago AP, eds. Clinical Strabismus Management. Philadelphia, PA: WB Saunders Co; 194.

Kirschen DG. Understanding sensory evaluation. In: Rosenbaum AL, San- tiago AP, eds. Clinical Strabismus Management. Philadelphia, PA: WB Saun- ders Co; 1999: 23.

Benegas NM, Egbert J, Engel WK, Kushner BJ. Diplopia secondary to anisei- konia associated with macular disease. Arch Ophthalmol. 1999;117(7):896- 899. Pratt-JohnsonJA,TillsonG.ManagementofStrabismusandAmblyopia:APrac- tical Guide. 2nd ed. New York, NY: Thieme; 2001. BielschowskyA.Congenitalandacquireddisruptionoffusion.AmJOphthalmol. 1935;18:925-937.

bismus Management, Kraft considers the terms synonymous but Kirschen4 states that the 2 terms “should not be con- fused.” Kushner and colleagues5 and Pratt-Johnson and Tillson6(p208) have also used the terms synonymously

The mutually exclusive definitions proposed by Bixen- man have not, to our knowledge, been articulated in the lit- erature but on careful review of the original descriptions we agree that there are advantages to differentiating between the 2 terms. Central fusion disruption can be con- sidered an acquired phenomenon in which bifoveal fusion is not possible. Horror fusionis (literally, fear of fusion) can be considered the active avoidance of bifoveal stimula- tion, as first stated by Bielschowsky.7 Although Biel- schowsky’s cases of horror fusionis had congenital strabis- mus, there is no reason to believe that the phenomenon cannot be observed in patients with central fusion disrup- tion. Horror fusionis is associated with characteristic syn- optophore speed effects in which an image swept across the retina of the nonfixing eye with constant velocity appears to speed up, then slow to a stop, then jump over the fixation target in the fixating eye.4 Pratt-Johnson and Tillson6 have described a similar “bobbing” phenomenon in patients with central fusion disruption.

Sashank K. Reddy, MD, PhD Cristian M. Salgado, MD David G. Hunter, MD, PhD

Author Affiliations: Department of Health Sciences and Technology, Massachusetts Institute of Technology, Bos- ton (Dr Reddy); Harvard Medical School, Boston, Mas- sachusetts (Dr Salgado); and Department of Ophthal- mology, Harvard Medical School, Children’s Hospital Boston, Boston, Massachusetts (Dr Hunter). Correspondence: Dr Hunter, Department of Ophthal- mology, Harvard Medical School, Children’s Hospital Bos- ton, 300 Longwood Ave, Boston, MA 02115 (david.hunter @childrens.harvard.edu).

Financial Disclosure: None reported.

 lished authoritative textbook on strabismus, Clinical Stra- 3

1. 2.

3.

4.

5.

6. 7.

Duke-Elder S. Aetiology of squint. In: Duke-Elder S, ed. System of Ophthal- mology. Vol VI. St Louis, MO: CV Mosby Co; 1976:243.

Von Noorden GK. Burian-von Noorden’s Binocular Vision and Ocular Motility: Theory and Management of Strabismus. 3rd ed. St Louis, MO: CV Mosby Co; 1985. KraftSP.Selectedexotropiaentitiesandprinciplesofmanagement.In:Rosen- baum AL, Santiago AP, eds. Clinical Strabismus Management. Philadelphia, PA: WB Saunders Co; 194.

Kirschen DG. Understanding sensory evaluation. In: Rosenbaum AL, San- tiago AP, eds. Clinical Strabismus Management. Philadelphia, PA: WB Saun- ders Co; 1999: 23.

Benegas NM, Egbert J, Engel WK, Kushner BJ. Diplopia secondary to anisei- konia associated with macular disease. Arch Ophthalmol. 1999;117(7):896- 899. Pratt-JohnsonJA,TillsonG.ManagementofStrabismusandAmblyopia:APrac- tical Guide. 2nd ed. New York, NY: Thieme; 2001. BielschowskyA.Congenitalandacquireddisruptionoffusion.AmJOphthalmol. 1935;18:925-93

There is nothing in the literature to suggest going gluten free will help with the above types of double vision, but this below link was interesting. 

https://www.verywellhealth.com/gluten-ataxia-symptoms-562398