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Brown syndrome is a rare eye disorder characterized by defects and errors in eye movement.

The disorder may be congenital (existing at or before birth), or secondary (for example, due to inflammation). Brown syndrome is caused by a malfunction of the superior oblique tendon, causing the eye to have difficulty moving upward, particularly during adduction (when eye turns towards the nose). In the United States, the prevalence of Brown syndrome is 1 in every 400450 strabismus cases. 35% of the patients with congenital Brown syndrome have a family member with Brown syndrome. This indicates Brown syndrome could potentially be a genetic trait. The syndrome occurs in women more than men. Of the people who have the syndrome in the United States, 59% are female and 41% male. In 55% of patients the syndrome is found only in the right eye, 35% only in the left eye, and 10% bilaterally. [edit]Background Brown syndrome was first documented by Harold W. Brown in 1950. He initially named it the "superior oblique tendon sheath syndrome". Since then, the name has changed, and the definition of the syndrome has become "limited elavation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye. Harold W. Brown characterized the syndrome in many ways such as Limited elevation in the eye when head is straight up

Eyes point out in a straight up gaze; greater separation of the upper and lower eyelids when the head is straight up Near normal elevation in adduction; and chin elevation for binocular fusion, to see one clear image instead of two blurry images He concluded that all of these features of Brown syndrome were due to the shortening or tightening of the anterior superior oblique tendon. Because this syndrome can be acquired or occur at random and has spontaneous resolution, Brown hypothesized one major truth for this disorder that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral inferior oblique muscle and secondary to a permanent shortening. After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of Brown's Syndrome. The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic. [edit]Types Brown syndrome can be divided in two categorizes based on the restriction of movement on the eye itself and how it effects the eye excluding the movement. [edit]Congenital

Brown Syndrome

Present at birth. It is the normal elevation of the eye into adduction, such that when the head is upright, adduction, the eye is in its normal position. With Brown Syndrome, there is an increase between the trochlea and the superior oblique tendon when the eye is straight up, causing them to position themselves differently. There are different types of congenital Brown Syndrome within each class. The first one, Halvestons theory of abnormal telescoping, forced, mechanism, is described as the tendon-slackening from its center attachment to the trochlea comes from a forced stretching of the central tendon. The stretching of the central tendon is mainly caused by the movement of the central tendon fibers. Another theory is the Wright hypothesis of congenital inelastic superior oblique muscle-tendon complex. This theory found that a tight or inelastic muscle-tendon complex was the best situation for a Brown's Syndrome patient. If the tendon was stretched about 250% there was a drop in elevation and the syndrome could be cured. Another fact from this experiment was that the attachment of the inferior orbital fibrous to the posterior glove would restrict eye movement. [edit]Acquired

Brown Syndrome

Acquired Brown Syndrome (Wright) may occur as a result of another pre-existing disorder or the stretching of the tendon sheath. Abnormal forcing mechanism explains a reduced lengthening of the superior oblique tendon is caused by stretching of the tendon sheath. Tight or inelastic superior oblique tendon describes how a tight superior oblique tendon can be caused. It is caused by a displacement of the tendon or a superior oblique tendon tuck. However, tissue built up around the superior oblique tendon could be a sign of thyroid disease or Hurler-Sheie syndrome. Brown Syndrome patients who have inflammatory conditions are described as having superior oblique click syndrome. Stenosing tenosynovitis or the trigger-thumb analogy theory is the most detailed theory for all acquired theories. In this theory the frequent movement of the superior oblique tendon can result in tendon swelling surrounding the tendon sheath. Scarring occurs around the trochlea because the anterior superior oblique tendon has limited movement causing Brown [edit]Characteristics There are some key characteristics of Brown syndrome that are not just obvious but also a disadvantage for the person. The first sign is when the chin points up and to the opposite side of the eye with the disorder. Another sign is when the head is straight up, the eye with the disorder is not aligned correctly in the eye socket, and is usually pointed at the nose because of the problems with the superior tendon sheath. Some other ones that are not so common and mentioned are; the eye does not move up in a straight up gaze, greater separation of the upper and lower eyelids when the head is straight up, the eye may be down shot when involved in adduction, there may also be some pain for the person with the syndrome. These characteristics are clear because they are on the outside of the body, which also makes them disturbing to the unknown. [edit]Causes There are a few classifications and potential causes for Brown syndrome. Congenital Brown Syndrome could be caused by an inelastic muscle-tendon complex, differences of the superior oblique tendon fibers, abnormal inferior orbital attachments, and the posterior orbital bands.

Brown syndrome has been researched more because it can be developed due to other diseases and disorders. A cause for scarring and adhesions is because during surgery you can receive scars from having a blepharoplasty, plastic surgery on the eyelid, and having fat removed. Reasons for the tightening or shortening of the superior oblique tendon are because of the muscles surrounding the tendon. An inelastic muscle would cause the tendon to shorten because its inflexible characteristic or a superior oblique tuck would because there is a section of the tendon removed. [edit]Treatments [edit]Medical

Care

There are a few procedures that can be done to fix Brown syndrome medically. When treating Brown syndrome with medical care the goal is to release the mechanical limitation to elevation in the eye. This can be solved by using anti-inflammatory medication. One approach is with ibuprofen. Another way to do this is to inject a steroid into the trochlea and oral corticosteroids. This is done because the trochlea and oral corticosteroids tend to limit movement and cause inflammation. [edit]Surgical

Care

The most effective method to fix Brown syndrome is by the use of surgical care. The most important indication for surgery is the presence of chin elevation or the eye not being positioned in its normal place when the head is straight up and down. The Wright silicone tendon expander technique can be used to fix chin elevation during adduction, head positioned normal, by lengthening the superior oblique tendon. This is done by performing tenotomy, cutting the tendon, and then inserting a segment of medical grade silicone 240 retinal band between the cut ends of the tendon. The problem with this procedure is that the silicone has to be placed within the tendon capsule without disrupting the floor of the tendon capsule. If this is done improperly the implant could be forced out of the tendon or the implant might attach to the outside of the tendon instead of holding the two tendons together. This procedure is very effective and is most commonly used when dealing with surgical repair. A few more methods to fix Brown syndrome include: the superior oblique split tendon lengthening technique, tenotomy, and superior oblique recession. The first method, superior oblique split tendon lengthening involves splitting the tendons on the section of the eye near the nose. This is done by removing the halves of the tendon, combining them together, and then eventually joining the halves that were made one onto the old tendon. The tendons are separated in a controlled manner and the superior oblique tendon remains as its original self. The reason this isnt used more often is because it weakens the tendon. By cutting the tendon in half and combining it, the tendon will never be its original self because the new tendon from the old halves is now longer and weaker. Tenotomy, cutting of the tendon, is done by using a 56mm stitching that keeps the already cut tendons from expanding too far. The main issue with this type of surgery is controlling the cut tendons from separating too far. This stitched bridge helps control the tendon but often causes under corrections. The rate of success for this procedure is 5085%.

The superior oblique recession technique creates a controlled slackening of the tendon. This is used the least compared to all of the other procedures because of its high rate of failure and chance for under corrections. More problems with this procedure include a change with the characteristics of the superior oblique tendon and possibly limited depression (Wright). Facial reconstruction is the final option to help patients with Brown syndrome. It is not recommend or used commonly because of the difficulty of the procedure and because of its low success rate. It is uncommonly used because freeing facial restrictions is usually unsuccessful. All procedures aim to align patients' eyes properly when they are in the primary position the ideal state.

Background
In 1950, Harold W. Brown first published on an unusual motility disorder, characterized by the following: limited elevation in adduction; divergence in straight upgaze (V-pattern); same degree of limitation on versions, ductions, and forced ductions; widening of the palpebral fissure on adduction; normal or near normal elevation in abduction; restricted forced ductions to elevation in adduction; and compensatory chin elevation for binocular fusion. Brown attributed the limited elevation to a short or tight anterior superior oblique tendon sheath. He termed this as superior oblique tendon sheath syndrome. The syndrome could be acquired or intermittent. In some cases, spontaneous resolution may occur. He further hypothesized that the short tendon sheath was due to a complete congenital paresis of the ipsilateral inferior oblique muscle and secondary to sheath contracture. In the early 1970s, Brown redefined the sheath syndrome with the following divisions: true sheath syndrome characterized only those cases that have a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome characterized all cases with the clinical features of a sheath syndrome caused by an anomaly other than a congenital short anterior sheath of the superior oblique tendon.[1] Clinical features of true and simulated sheath syndromes were similar, but true sheath syndrome was always congenital and constant without spontaneous recovery. In the mid 1970s, Parks and colleagues reported that a tight tendon sheath was not the cause of Brown syndrome; instead, it was a tight or short superior oblique tendon.[2] Subsequent studies confirmed the cause of the syndrome to be a tight or inelastic superior oblique tendon. Brown syndrome can be divided into congenital and acquired.

Congenital Brown syndrome


Superior oblique Brown syndrome Superior oblique Brown syndrome or true Brown syndrome is restriction of eye movement up and adduction caused by an abnormal superior oblique muscle or tendon. As originally demonstrated by Brown, normal elevation of the eye into adduction increases the distance between the trochlea and the superior oblique insertion as the eye moves up and into adduction. A tight or inelastic superior oblique tendon muscle complex would restrict ocular elevation in adduction. Many theories for the cause of the tight or inelastic tendon exist. Etiology of superior oblique Brown syndrome Helveston theory of abnormal telescoping mechanism o Until recently, it was believed that the superior oblique tendon moves through the trochlea much like a rope through a pulley. Through a detailed anatomical study, Helveston showed that the tendon-slackening distal to the trochlea comes from a telescoping elongation of the central tendon.[3] o Telescoping elongation of the tendon is due to movement of the central tendon fibers, which have scant interfiber connections.

o Congenital Brown syndrome could be caused by a developmental abnormality of the elastic-crossed fibers that normally allow the telescoping movement of the central tendon fibers. Wright hypothesis of congenital inelastic superior oblique muscle-tendon complex o In 1999, Wright described a computer simulation of Brown syndrome, using two specific models, as follows: (1) a short superior oblique tendon, and (2) a stiff superior oblique tendon (stretched sensitivity). The computer model showed that a tight or inelastic muscle-tendon complex was the best fit for the Brown syndrome pattern of deviation. o The best simulation of Brown syndrome was obtained with 250% stretched sensitivity, producing a -4 limitation of elevation in adduction and a -1 limitation of elevation in abduction. With this simulation of a stiff superior oblique muscle-tendon complex, there was a very small deviation in primary position and no deviation in downgaze, which is consistent with the clinical findings of Brown syndrome. o Shortening the tendon from 32 mm to 28 mm did not significantly limit the elevation in adduction; however, shortening the tendon to 22 mm created a -4 limitation of elevation in adduction. Shortening the tendon to 22 mm also caused a hypotropia of 11 prism diopters (PD) in primary position and a hypotropia of 7 PD in downgaze, which is inconsistent with the classic clinical findings of Brown syndrome, where the deviation in primary position is very small to nonexistent and there is no hypotropia in downgaze. o Thus, the best computer model for Brown syndrome is a stiff or inelastic muscle-tendon complex. Perhaps, congenital Brown syndrome is a form of congenital fibrosis of the superior oblique muscle, which results in a stiff or inelastic muscle-tendon complex.[4] Nonsuperior oblique Brown syndrome Nonsuperior oblique Brown syndrome or pseudo-Brown syndrome is a restriction of ocular elevation in adduction caused by pathology other than an abnormality of the superior oblique muscle or tendon. Etiology of congenital nonsuperior oblique Brown syndrome Congenital bands: Inferior orbital fibrous adhesions or fibrous bands to the posterior globe are rare causes of restriction of elevation in adduction. Congenital inferior location of lateral rectus muscle pulley: Rare case of congenital Brown syndrome are caused by congenital inferior location of the lateral rectus muscle. In these cases, the limitation of elevation in adduction is caused by the stiff lateral rectus muscle that is congenitally located inferior to the normal position.[5]

Acquired Brown syndrome


Acquired superior oblique Brown syndrome See Causes. Etiology of acquired superior oblique Brown Syndrome Abnormal telescoping mechanism: In constant or intermittent acquired Brown syndrome, reduced telescoping elongation of the superior oblique tendon would be due to one of the following: vascular dilatation of the tendon sheath vessels and local edema occurring within the confined area of the trochlea. Tight or inelastic superior oblique tendon o A tight superior oblique tendon can be caused by a mass that displaces the tendon, a scleral buckling, or a superior oblique tendon tuck. o A rare acquired fibrosis of the superior oblique muscle is possibly associated with thyroid disease, an intramuscular injection of local anesthetic, or Hurler-Scheie syndrome. Acquired short tendon: This condition could be caused by a superior oblique tendon tuck, a mass that displaces the tendon, or a scleral buckling. Superior oblique click syndrome o This theory has been used to explain acquired Brown syndrome that is associated with inflammatory conditions. o Inflammation produces a nodule on the superior oblique tendon, just posterior to the trochlea. The nodule would have difficulty entering the trochlea, thus restricting tendon movement.

Stenosing tenosynovitis (trigger-thumb analogy theory) o Chronic movement of the superior oblique tendon through the trochlea can result in a traumatic tenosynovitis with tendon-swelling and stenosis of the surrounding tendon sheath. o Trigger-thumb is a congenital or acquired constriction or stenosis of the fibrous sheath, which surrounds the tendon and causes secondary enlargement of the tendon proximal to the constriction. o The combination of a sheath-stenosis and tendon swelling prevents movements of the tendon. Peritrochlear scarring o Scarring or fibrosis around the trochlea and the anterior superior oblique tendon would restrict the tendon movement, causing Brown syndrome. o Extensive scarring around the trochlea can result in restriction of the tendon movement in both ways, resulting in both a Brown syndrome and a superior oblique palsy (canine tooth syndrome). This can be caused by trauma, periocular surgery, and upper lid blepharoplasty with removal of periorbital fat with cautery.

Acquired nonsuperior oblique Brown syndrome


Etiology of acquired nonsuperior oblique Brown syndrome Acquired nonsuperior oblique etiologies: Inferior orbital fibrous adhesions to the posterior globe are caused by the following: orbital floor fracture and fat adherence syndrome associated with inferior orbital trauma. Superior nasal orbital mass: These patients usually demonstrate a large vertical deviation in primary position often associated with exotropia. Possible causes are a glaucoma drainage implant or a neoplasm in the superior orbital quadrant. Scarring in the inferior temporal anterior orbit to the globe will cause a pattern of restriction that looks very similar to Brown syndrome with restriction of elevation in adduction. Unlike superior oblique Brown syndrome, there is also restriction to adduction. The author had seen this with scarring and fat adherence after transconjunctival blepharoplasty. Orbital floor fracture can rarely cause a restriction of elevation that looks like Brown syndrome. In these cases, a similar elevation defect in adduction and abduction is present.

Frequency
United States Frequency of this condition is 1 in 400-450 strabismus cases. Although familial Brown syndrome appears to be rare, Wright showed that 35% of patients with congenital Brown syndrome had a family member with amblyopia or strabismus.[4] This finding might indicate the presence of an underlying genetic trait. International Same as in the United States.

Mortality/Morbidity
Amblyopia, strabismus, and an abnormal head position may be findings from Brown syndrome.

Race
No racial predilection exists.

Sex
In Brown's classic study of 126 patients, he reported that there was a higher incidence of the syndrome in females (59%) than in males (41%). A right-eye bias also occurred; involvement was 55% in right eyes, 35% in left eyes, and 10% bilateral.

Wright found 5% of bilateral cases and analyzed the male-female distribution of Brown syndrome according to different subgroups: congenital Brown syndrome (almost identical sex distribution), idiopathic acquired Brown syndrome (63% females), and traumatic acquired Brown syndrome (82% males).[4] Diplopia may occur when the patient looks up and to the contralateral side of the affected eye. Patients with congenital Brown syndrome rarely complain of diplopia, because most patients have developed suppression. Patients with acquired Brown syndrome in late childhood or adulthood experience diplopia when tropic. Pain Some patients with acquired Brown syndrome present with inflammatory signs. These signs include supranasal orbital pain, tenderness, intermittent limitation of elevation in adduction, and pain that is associated with this ocular movement. Characteristic physical findings include the following: Limited elevation in adduction, an invariable sign, is the hallmark of Brown syndrome. The amount of limited elevation in adduction can range from minimal (-1) to severe (-4). The severe form has been termed Brown plus. Even in severe cases of congenital Brown syndrome, there is minimal hypotropia in primary position and no hypotropia in downgaze. A significant limitation of elevation in abduction is present in 70% of patients, but it is the difference between elevation in adduction versus elevation in abduction that differentiates Brown syndrome from such disorders as double elevator palsy (where elevation is equal to or worse in abduction). A lack of significant hypotropia in primary position in cases of nontraumatic Brown syndrome has been observed. In contrast, much larger hypotropias have been observed in cases of Brown syndrome associated with trauma or periorbital surgery. If the vertical deviation in primary position is greater than 10-12 PD, consider an inferior oblique palsy, severe periocular scarring, or a superior nasal mass; do not consider Brown syndrome caused by a tight or inelastic superior oblique tendon. Patients often present with compensatory head-posturing, their chin up, and a contralateral face turn to avoid the hypotropia that increases in upgaze and gaze to the contralateral side of the affected eye. Amblyopia can occur in patients with Brown syndrome, but the incidence compared with the general population is low in most patients with good binocular fusion. Minimal or no superior oblique overaction and positive forced ductions up and in are present. The presence of even mild superior oblique overaction should be regarded with suspicion, since this finding is inconsistent with Brown syndrome of superior oblique tendon etiology. A feature that often is associated with acquired Brown syndrome is an audible or palpable superior nasal click on ocular rotations up and nasalward; sometimes, the pain is associated with this ocular movement. Digital pressure in the area of the trochlea can unlock and improve ocular rotations in some cases. Contralateral pseudoinferior oblique overaction occurs because of the limited elevation in abduction. o Because of the Hering law of yoke muscles, increased innervation to the contralateral inferior oblique muscle occurs as the eye with Brown syndrome tries to elevate and abduct. o Apparent inferior oblique overaction disappears when the superior oblique restriction is relieved. The positive forced ductions maneuver is a critical part of the syndrome; it equals the limitation that is seen on ductions and versions. A positive forced ductions test, by itself, does not indicate a tight superior oblique muscle tendon as the cause of Brown syndrome. Nonsuperior oblique restrictions (eg, inferior orbital adhesions) can restrict ocular elevation in adduction. Objective fundus torsion: In Brown syndrome secondary to a tight superior oblique tendon, intorsion occurs as the eye moves up and encounters the tight superior oblique tendon. Clinically, no torsion occurs in primary position or downgaze, but intorsion in upgaze does occur. Fundus torsion is shown in the

images below.

Fundus torsion (direct view). The bottom set of fundus photographs represents downgaze; the center photographs, primary position; and the top photographs, upgaze. Note that in the top set of photographs, the left fundus is intorted as the foveal fixation is slightly above the top of the optic disc. Courtesy of Kenneth Wright, MD.

The images below show acquired Brown syndrome. A 3-year-old patient with acquired right Brown syndrome. Marked limitation of elevation in adduction is present in the right eye. Pseudo-

overaction of the left inferior oblique is present. Courtesy of Kenneth Wright, MD. The same patient as in the image above, 6 years later. The patient shows normal eye movements, and no signs of Brown syndrome. A spontaneous resolution occurred over a 2-year period. Courtesy of Kenneth Wright, MD.

Composite photographs, showing left Brown syndrome with marked limitation of elevation in adduction. Courtesy of Kenneth Wright, MD.

The classification/potential causes of Brown syndrome are as follows: Congenital onset Congenital Brown syndrome Inelastic muscle-tendon complex (Wright hypothesis) Anomalies of the superior oblique tendon fibers o Congenital pseudo-Brown syndrome Anomalous inferior orbital adhesions Posterior orbital bands Acquired onset o Acquired Brown syndrome Peritrochlear scarring and adhesions - Chronic sinusitis, trauma (superior temporal orbit), blepharoplasty and fat removal, and lichen sclerosus et atrophicus and morphea Tendon-trochlear inflammation and edema - Idiopathic inflammatory (pain and click), trochleitis with superior oblique myositis, acute sinusitis, adult rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, possibly distant trauma (cardiopulmonary resuscitation [CPR] and long bone fractures), and possibly postpartum hormonal changes Superior nasal orbital mass - Glaucoma implant and neoplasm o

Tight or inelastic superior oblique muscle - Thyroid disease (inelastic muscle), peribulbar anesthesia (inelastic tendon), Hurler-Scheie syndrome (inelastic tendon), and superior oblique tuck (short tendon) Idiopathic o Acquired pseudo-Brown syndrome Floor fracture Retinal band around inferior oblique muscle Inferior temporal adhesions MRI AND LABORATORIUM No laboratory tests are specifically required in the workup of congenital Brown syndrome. In cases of acquired, nontraumatic Brown syndrome, tests to exclude autoimmune diseases, such as lupus, juvenile rheumatoid arthritis (JRA), and rheumatoid arthritis, may need to be ordered. Consider MRI of the orbit for acquired Brown syndrome, especially if associated with pain, discomfort, signs of inflammation, or an atypical pattern of strabismus. In some cases, imaging studies may identify pathology in the area of the trochlea, even superior nasal orbital tumors and sinusitis.

Medical Care
Spontaneous resolution of Brown syndrome rarely occurs; if it does, it is more likely in nontraumatic acquired cases. Because of the possibility for late spontaneous recovery, a conservative approach to management is justified, especially for patients with nontraumatic acquired cases. Patients with acquired Brown syndrome should be evaluated medically for coexisting systemic disease. o If a disorder, such as rheumatoid arthritis or sinusitis, is identified, treat accordingly. o Once systemic disease is excluded, patients who have acquired Brown syndrome with signs of inflammation can be treated with anti-inflammatory medication. Oral ibuprofen is a good first-line choice. Local steroid injections in the area of the trochlea and oral corticosteroids can be used for inflammation. o Once the inflammatory disease process is controlled, patients with inflammatory Brown syndrome may show spontaneous resolution. Congenital Brown syndrome is unlikely to improve spontaneously; therefore, surgery is important to consider as an option.

Surgical Care
The most important indications for surgery are the presence of chin elevation and severe limitation of elevation in adduction, which significantly interferes with the quality of life. Acquired nontraumatic cases should be observed conservatively, because spontaneous resolution may occur. Consider surgery for longstanding cases. The treatment of superior oblique Brown syndrome is to lengthen the tendon and release the restriction without causing a superior oblique palsy. The first phase is to identify the restriction's cause, inelastic superior oblique tendon or no superior oblique tendon (eg, fat adhesion). The most important signs of inelastic tendon etiology include positive forced duction that is worse with retropulsion, intorsion in upgaze, and negative forced duction after transecting the superior oblique tendon. The best surgical procedures lengthen the tendon rather than severing the tendon. The old procedure of tenotomy was associated with 50-80% risk for iatrogenic superior oblique palsy. The surgically caused superior oblique palsy is worse than the Brown syndrome in many cases. Wright silicone tendon expander technique (preferred method) o This technique consists of elongating the superior oblique tendon by performing a tenotomy and then of inserting a segment (about 5 mm) of medical-grade silicone 240 retinal band between the cut ends of the tendon. o Silicone must be placed within the tendon capsule without disrupting the floor of the tendon capsule; otherwise, complications, such as postoperative adherence of the silicone to the sclera or spontaneous extrusion of the implant, may occur.

o This technique has been effective. o The silicone tendon expander procedure is not easy to perform because tenotomy or tenectomy requires special surgical techniques. o Preoperative and postoperative images of a patient who underwent the silicone tendon

expander procedure are shown below.

This patient has the longest follow-up in the silicone tendon expander group at 11 years. A. Preoperative composite photograph of eye movements, showing right Brown syndrome. The patient underwent silicone tendon expander, 6 mm right eye. B. Postoperative photograph 3 years after surgery, showing full ocular motility. C. Postoperative photograph 11 years after surgery, showing continued normal ocular motility. Courtesy of Kenneth Wright, MD.

Superior oblique split tendon lengthening technique o This technique splits the tendon on the nasal side of the superior rectus muscle. The halves of the tendon are removed and then joined to lengthen the tendon. o The function of the superior oblique tendon remains intact and the cut tendon ends are separated in a controlled manner. Suture bridge o A nonabsorbable suture is placed to connect the cut ends of the superior oblique tendon, thus preventing a consecutive superior oblique palsy. o The suture bridge can act as a scaffold for scar that can reunite the cut tendon ends, thus resulting in an undercorrection with a significant residual Brown syndrome. Tenotomy o This treatment has been relatively successful for primary superior oblique overaction in nonfusing patients. However, patients with bifoveal fusion do not tolerate induced postoperative cyclovertical deviations. o A major problem with this technique is the uncontrolled separation of tendon ends. o The incidence of postoperative superior oblique paresis is reported to be 50-80%. o Parks and Eutis added a simultaneous ipsilateral inferior oblique recession with a superior oblique tenotomy to reduce the incidence of a secondary superior oblique palsy.[6] o Use of a 5-6 mm suture bridge can keep the cut tendon ends from separating too much. Unfortunately, this suture bridge can act as scaffolding for fibrosis to reunite the cut tendon ends, resulting in undercorrections. Superior oblique recession o This procedure produces a graded slackening of the tendon. o The results are mixed, because undercorrections are common. o The problem with recessing the superior oblique tendon is that it dramatically changes the characteristics of the superior oblique tendon insertions and alters its functional mechanics. This results in the postoperative complication of limited depression. Superior oblique and trochlear luxation consists of removing the tendon from the trochlea by luxating the trochlea. This procedure has been abandoned. Sheathectomy has been abandoned.