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| LETTER TO EDITOR |
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| Year : 2017 | Volume
: 10
| Issue : 2 | Page : 128-130 |
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Resolution of acquired Brown syndrome with oral steroid therapy
Preeti Patil Chhablani, Anjali Chandrasekharan
Jasti V Ramanamma Children's Eye Care Center, L. V. Prasad Eye Institute, Hyderabad, Telangana, India
| Date of Web Publication | 29-Jun-2017 |
Correspondence Address:
Preeti Patil Chhablani
Jasti V Ramanamma Children's Eye Care Center, L. V. Prasad Eye Institute, Kallam Anji Reddy Campus, Hyderabad, Telangana
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ojo.OJO_4_2016
How to cite this article:
Chhablani PP, Chandrasekharan A. Resolution of acquired Brown syndrome with oral steroid therapy. Oman J Ophthalmol 2017;10:128-30 |
Sir,
Brown syndrome has been an enigma for clinicians and scientists alike, ever since Harold Brown first described the constellation of distinct ocular motility findings characterized by limited elevation in adduction. In terms of etiology, Brown syndrome has two distinct forms – congenital and acquired. While the congenital variety is primarily considered to be caused by abnormalities of the trochlea or the tendon sheath of the superior oblique,[1],[2] newer theories now consider Brown syndrome to be a part of congenital cranial dysinnervation syndromes.[3] Acquired Brown syndrome may be a result of a large variety of conditions affecting the trochlea, tendon sheath, tendon, or peritrochlear tissue. While many of these cases are idiopathic, some may be associated with systemic inflammatory conditions such as rheumatoid arthritis and systemic lupus erythematosus or with localized inflammation in the absence of obvious systemic disease. Other causes of acquired Brown syndrome include mass lesions in the superior oblique tendon, iatrogenic Brown syndrome following superior oblique tuck surgeries, or after fat adherence syndrome following inferior oblique weakening procedures, sinus surgeries, restrictive pathologies such as thyroid ophthalmopathy and trauma.[1]
We present our experience with one such case. A 9-year-old female child presented to our clinic with a history of sudden onset of vertical binocular double vision in upgaze, associated with pain on attempted upgaze. There was no history of trauma, any previous surgery, any systemic illnesses, joint pain, skin rashes, or fever. On examination, she had a chin up posture with a left head tilt. Her visual acuity was 20/20, N6 in both eyes. Ocular motility examination showed -5 limitation of elevation in adduction in the left eye, which reduced in straight upgaze and in abduction [Figure 1]. There was tenderness on palpation over the left trochlear area. The anterior segment and fundus examination was normal. Magnetic resonance imaging orbit with contrast was advised and did not show any mass lesion or evidence of inflammation in the trochlear region. The complete blood count was within normal limits; rheumatoid factor, antineutrophilic antibody levels, antineutrophil cytoplasmic antibodies levels, erythrocyte sedimentation rate, and C-reactive protein levels were all within normal limits. We prescribed a course of oral prednisolone (1 mg/kg) with a weekly taper. She was followed up every 2 weeks. With 2 days of steroid treatment, the patient reported a decrease in pain and the motility completely normalized in 2 months [Figure 2]. | Figure 1: Right eye showing elevation deficit in adduction which decreases in straight upgaze and in abduction
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 | Figure 2: Complete resolution of Brown syndrome in the right eye following oral steroid therapy
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In conclusion, management of acquired Brown syndrome depends on the underlying pathology. While spontaneous resolution has been reported,[1],[4] patients presenting with pain and signs of inflammation are usually treated with oral steroids, oral nonsteroidal anti-inflammatory drugs, or perilesional steroid injections.[4] Detailed systemic investigations are required to rule out underlying inflammatory or connective tissue disorders, and treatment of any such detected disorder should be undertaken. Most cases resolve with anti-inflammatory therapy; however, local injections may be needed in refractory cases.[4] Rarely, surgical weakening of the superior oblique may be required after documenting stability of the deviation.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
| 1. | Wright KW. Brown's syndrome: Diagnosis and management. Trans Am Ophthalmol Soc 1999;97:1023-109.  [ PUBMED] |
| 2. | Wilson ME, Eustis HS Jr., Parks MM. Brown's syndrome. Surv Ophthalmol 1989;34:153-72. |
| 3. | Coussens T, Ellis FJ. Considerations on the etiology of congenital Brown syndrome. Curr Opin Ophthalmol 2015;26:357-61. |
| 4. | Lee J. Management of Brown syndrome. Semin Ophthalmol 2008;23:291-3. |
[Figure 1], [Figure 2]
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