AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Pathophysiology

Brown syndrome can be divided into congenital and acquired.

Congenital Brown syndrome

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.

Helveston theory of abnormal telescoping mechanism

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

Telescoping elongation of the tendon is due to movement of the central tendon fibers, which have scant inter-fibers connections.

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

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.   

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. 

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. 

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

Congenital nonsuperior oblique tendon etiology

Inferior orbital fibrous adhesions to the posterior globe would limit the eye movement. This could be caused by congenital bands.

Acquired Brown syndrome

See Causes.

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

A tight superior oblique tendon can be caused by a mass that displaces the tendon, a scleral buckling, or a superior oblique tendon tuck.

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

This theory has been used to explain acquired Brown syndrome that is associated with inflammatory conditions.

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)

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.

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.

The combination of a sheath-stenosis and tendon swelling prevents movements of the tendon.

Peritrochlear scarring

Scarring or fibrosis around the trochlea and the anterior superior oblique tendon would restrict the tendon movement, causing Brown syndrome.

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 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.

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

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• 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.

Physical

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.
• • 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.
  • 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.

Causes

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
  • Congenital pseudo-Brown syndrome
  • • Anomalous inferior orbital adhesions
    • Posterior orbital bands
• Acquired onset
• • 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
    • 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
  • Acquired pseudo-Brown syndrome
  • • Floor fracture
    • Retinal band around inferior oblique muscle
    • Inferior temporal adhesions

DIFFERENTIALS

Section 4 of 11  

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• References

Other Problems to be Considered

The following signs of superior oblique overaction help differentiate it from Brown syndrome (see Table below):

• Mild limitation of elevation in adduction
• No limitation of elevation in abduction
• Common bilateral involvement
• Superior oblique overaction
• A-pattern, lambda-subtype with divergence in downgaze
• Fundal examination reveals intorsion in primary position that increases in downgaze.
• Negative forced ductions test

The following signs occur with inferior oblique paresis, differentiating it from Brown syndrome (see Table below):

• Limitation of elevation in adduction occurs, with a large vertical deviation in primary position, usually more than 10 PD.
• Marked superior oblique overaction
• A-pattern, convergence in upgaze
• Fundal examination reveals intorsion in primary position, which increases in upgaze.
• Positive head-tilt test
• Negative forced ductions test

Double elevator palsy: In Brown syndrome, limitation of elevation in adduction is invariable; yet, this sign is also present in 70% of patients with double elevator palsy. The difference between elevation in adduction versus elevation in abduction differentiates Brown syndrome from double elevator palsy, where elevation is equal to or worse in abduction.

Differential Diagnoses: Clinical Features of Brown Syndrome, Inferior Oblique Paresis, and Superior Oblique Overaction

WORKUP

Section 5 of 11  

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Lab Studies

• 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.

Imaging Studies

• 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.

TREATMENT

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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.
• • If a disorder, such as rheumatoid arthritis or sinusitis, is identified, treat accordingly.
  • 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.
  • 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 long-standing cases.

Treatment of Brown syndrome should 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.

• Wright silicone tendon expander technique (preferred method)
• • This technique consists of elongating the superior oblique tendon by performing a tenotomy and then of inserting a segment of medical-grade silicone 240 retinal band between the cut ends of the tendon.
  • 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.
  • This technique has been effective.
  • The silicone tendon expander procedure is not easy to perform because tenotomy or tenectomy requires special surgical techniques.
• Superior oblique split tendon lengthening technique
• • 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.
  • The function of the superior oblique tendon remains intact and the cut tendon ends are separated in a controlled manner.
  • The author has used this procedure on one patient with excellent results.
• Tenotomy
• • 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.
  • A major problem with this technique is the uncontrolled separation of tendon ends.
  • The incidence of postoperative superior oblique paresis is reported to be 50-85%.
  • 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.⁵
  • 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
• • This procedure produces a graded slackening of the tendon.
  • The results are mixed, because undercorrections are common.
  • 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 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.

Consultations

Consult a rheumatologist in acquired nontraumatic cases.

MEDICATION

Section 7 of 11  

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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs)

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

FOLLOW-UP

Section 8 of 11  

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Complications

• Patients should be observed for recurrence of amblyopia, strabismus, and abnormal head position.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Early detection to prevent amblyopia

MULTIMEDIA

Section 10 of 11  

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Media file 1:  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.
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Media type:  Photo

Media file 2:  The same patient as in Media file 1, 6 years later. The patient shows normal eye movements, no signs of Brown syndrome. A spontaneous resolution occurred over a 2-year period. Courtesy of Kenneth Wright, MD.
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Media type:  Photo

Media file 3:  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.
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Media type:  Photo

Media file 4:  Composite photographs, showing left Brown syndrome with marked limitation of elevation in adduction. Courtesy of Kenneth Wright, MD.
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Media type:  Photo

Media file 5:  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.
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Media type:  Photo

REFERENCES

Section 11 of 11

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• References

1. Brown HW. True and simulated superior oblique tendon sheath syndromes. Doc Ophthalmol. Feb 21 1973;34(1):123-36. [Medline].
2. Parks MM, Brown M. Superior oblique tendon sheath syndrome of Brown. Am J Ophthalmol. Jan 1975;79(1):82-6. [Medline].
3. Helveston EM, Merriam WW, Ellis FD, Shellhamer RH, Gosling CG. The trochlea. A study of the anatomy and physiology. Ophthalmology. Feb 1982;89(2):124-33. [Medline].
4. Wright KW. Brown's syndrome: diagnosis and management. Trans Am Ophthalmol Soc. 1999;97:1023-109. [Medline].
5. Parks MM. Bilateral superior oblique tenotomy for A-pattern strabismus in patients with fusion (commentary). Binoc Vis. 1988;3:39.
6. Buckley EG, Flynn JT. Superior oblique recession versus tenotomy: a comparison of surgical results. J Pediatr Ophthalmol Strabismus. May-Jun 1983;20(3):112-7. [Medline].
7. Clarke MP, Bray LC, Manners T. Superior oblique tendon expansion in the management of superior oblique dysfunction. Br J Ophthalmol. Jul 1995;79(7):661-3. [Medline].
8. Clarke WN, Noel LP. Brown's syndrome with contralateral inferior oblique overaction: a possible mechanism. Can J Ophthalmol. Aug 1993;28(5):213-6. [Medline].
9. George JL, Maalouf T, Cordonnier MO, Angioi-Duprez K. [Abnormal eyelid positions in Brown syndrome]. J Fr Ophtalmol. Jun 2004;27(6 Pt 1):579-87. [Medline].
10. Helveston EM, Birchler C. Superior oblique palsy: subclassification and treatment suggestions. Am Orthopt J. 1982;32:104-110.
11. Prieto-Diaz J. Posterior tenectomy of the superior oblique. J Pediatr Ophthalmol Strabismus. Sep-Oct 1979;16(5):321-3. [Medline].
12. Scott AB, Knapp P. Surgical treatment of the superior oblique tendon sheath syndrome. Arch Ophthalmol. Sep 1972;88(3):282-6. [Medline].
13. Scott WE, Jampolsky AJ, Redmond MR. Superior oblique tenotomy: indications and complications. Int Ophthalmol Clin. 1976;16(3):151-9. [Medline].
14. Von Noorden GK. Binocular Vision and Ocular Motility. St. Louis: CV Mosby; 1996:437-442.
15. Wright KW. Color Atlas of Ophthalmic Surgery-Strabismus. Philadelphia, Pa: Lippincott; 1991:201-219.
16. Wright KW. Superior oblique silicone expander for Brown syndrome and superior oblique overaction. J Pediatr Ophthalmol Strabismus. Mar-Apr 1991;28(2):101-7. [Medline].
17. Wright KW. Surgical procedure for lengthening the superior oblique tendon. Invest Ophthamol Vis Sci. 1989;30(sup):377.
18. Wright KW, Min BM, Park C. Comparison of superior oblique tendon expander to superior oblique tenotomy for the management of superior oblique overaction and Brown syndrome. J Pediatr Ophthalmol Strabismus. Mar-Apr 1992;29(2):92-7; discussion 98-9. [Medline].
19. Wright KW, Silverstein D, Marrone AC, Smith RE. Acquired inflammatory superior oblique tendon sheath syndrome. A clinicopathologic study. Arch Ophthalmol. Nov 1982;100(11):1752-4. [Medline].

Article Last Updated: Dec 3, 2007