Strabismus Online Information Resource

Brown syndrome




  • In 1950, Brown reported a motility disorder characterised mainly by deficient elevation of the eye in adduction. Originally it was termed superior oblique tendon sheath syndrome. It is now known as Brown's syndrome.

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Clinical features

  • deficient elevation in adduction
  • less elevation deficiency in midline
  • minimal or no elevation deficit in abduction
  • minimal or no superior oblique overaction
  • divergence in upgaze producing a V-pattern
  • positive forced duction testing
  • downshoot in adduction
  • widened palpebral fissure in adduction
  • anomalous head posture: chin-up &/or face-turn away from affected eye
  • primary position hypotropia

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  • congenital vs acquired
  • constant vs intermittent
  • severity:
    • mild: deficient elevation in adduction no hypotropia or downshoot in adduction
    • moderate: deficient elevation and downshoot in adduction no hypotropia in primary position
    • severe: deficient elevation and downshoot in adduction hypotropia present in primary position commonly associated with an abnormal head posture

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  • Brown's syndrome occurs in 10 to 24 % of vertical muscle anomalies.
  • The right eye is more commonly affected than the left eye.
  • Females have a greater incidence than males (3:2).

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  • Brown called it superior oblique tendon-sheath syndrome thinking it was caused by a shortened anterior sheath of superior oblique tendon; this theory has been shown to be incorrect.

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Acquired form

  • Disturbance of free tendon movement through the trochlear pulley (i.e. a stenosing tenosynovitis of the trochlea).
  • Usually intermittent and associated with an audible "click".
  • Associated with inflammation and trauma such as rheumatoid arthritis, juvenile arthritis, collagen vascular diseases, trochlear bursitis, sinus surgery, orbit or muscle surgery, scleral buckling and glaucoma implant surgery.
  • Canine tooth syndrome refers to a posttraumatic condition that produces scarring in the trochlear region such that movement of the tendon in either direction is restricted producing a combined Brown`s syndrome and superior oblique palsy.

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Congenital form

  • It is possibly secondary to a short and inelastic superior oblique muscle and tendon.
  • Inflammation, trauma and stenosis may be contributing factors.
  • Fibrous adhesions may be present around the trochlear area.
  • Spontaneous resolution is possible and improvement can occur in time.

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  • Observation alone is the most common suggested management for all forms of Brown's syndrome.
  • Spontaneous regression is common in acquired and intermittent cases and less common in congenital and constant cases.
  • Motion eye exercises and local/systemic steroids have been showed to improve the condition in selected patients.
  • If Brown's syndrome occurs in association with a systemic inflammatory disease, resolution can occur when the systemic disease is in remission.
  • Surgery is usually indicated for primary position hypotropia and/or anomalous head posturing.
    • Superior oblique tenotomy is effective but produces a superior oblique palsy with overacting ipsilateral inferior oblique 44 to 82% of the time.
    • Superior oblique recession nasally using a silicone spacer (Wright) is also effective and avoids this complication.

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

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