420
J Oral Maxdlofac
ACQUIRED BROWN’S SYNDROME: IATROGENIC CAUSES
Surg
40:42@424,1990
Acquired Brown’s Syndrome: la trogenic Causes V. ILANKOVAN, FDSRCS, FRCS(ED),* LA. AL-QURAINY, MB, CHB, MCOPHTH, DO,t K.F. MOOS, FDSRCS, FRCS(ED),$- AND G.N. DUTTON, MD, FRCS§
Brown’s syndrome, or superior oblique tendon sheath syndrome, is a restrictive ocular motility disorder in which there is impairment of free movement of the tendon of this muscle through the trochlea. It was described in 1950 by Brown,’ who later classified it into true and simulated forms.’ The former is always due to a congenital cause, whereas the simulated form can be either congenital or acquired.* The disorder is characterised by restriction of elevation of the eye on adduction associated with a positive forced duction test in that direction. Elevation in the primary position of gaze is normal or near normal. Other features include widening of the palpebral fissure on adduction and, occasionally, minimal overaction of the ipsilateral superior oblique muscle.3 Many acquired causes have been described in the literature. Stenosing tenosynovitis,4 rheumatoid arthritis,’ and adjacent sinusitis6 comprise inflammatory causes, whereas injury’.* and surgical blepharoplasty’ have been implicated as traumatic causes. Metastatic deposits may also give rise to this condition.” We report two cases in which surgical procedures in the region of the trochlea have resulted in Brown’s syndrome.
Received from Canniesburn Hospital, Bearsden, Glasgow, UK; and Tennent Institute of Ophthalmology, Western Infirmary, Glasgow, UK. * Reeistrar in Oral and Maxillofacial Surgerv. _ _ t Research Fellow. $ Consultant in Oral and Maxillofacial Surgery. § Consultant in Ophthalmology. Address correspondence and reprint requests to Mr Ilankovan: Department of Oral and Maxillofacial Surgery, Canniesburn Hospital, Bearsden, Glasgow G61 IQL, UK. 0 1990 American
Association
geons 0278-2391/90/4804-0018$3.00/0
of Oral and Maxillofacial
Sur-
Report of Two Cases Case 1 A 22-year-old woman was involved in a traffic accident in November 1982; she sustained lacerations to both her upper eyelids and supraorbital regions. The wounds were repaired in the casualty department. Since then, two further plastic surgical procedures have been carried out to revise the scars and to remove fragments of glass from the left supraorbital region. The patient did not initially have any visual symptoms. However, early in 1988, an infection around the right medial canthal region raised the suspicion of a retained foreign body. The area was explored, but no foreign body was found. When the patient was subsequently reexamined, she complained of double vision and difficulty in focusing. An ophthalmic opinion was sought. Examination revealed impairment of elevation of the right eye on adduction associated with diplopia. The forced duction test in the direction of impairment was positive. Hess screen charts (Fig 1) supported this finding, and a diagnosis of acquired Brown’s syndrome was made. This was thought to be due to scarring around the right trochlea following the exploratory surgery, which had prevented free movement of the superior oblique tendon through the trochlea. No treatment was carried out because the field of binocular single vision was wide and central.
Case 2 A 21-year-old man with congenital hypertelorism underwent various subcranial surgical procedures between 1980 and 1988. The most recent operation involved bilateral malar osteotomies with bone grafting via a bicoronal flap. Within a week after the operation the patient complained of double vision for the first time. Radiographs failed to show any abnormality. An ophthalmic opinion was sought, and examination revealed unaided visual acuities of 20/16.7 for each eye. In slight depression he had no double vision, but there was a demonstrable latent divergence and a slight left hyperphoria. This broke down into a vertical squint with divergence on upgaze to the left, requiring a 3-diopter base-up prism before the left eye to correct the diplopia. This indicated that the patient had an antecendent esophoria which became an esotropia on elevation due to loss of fusion resulting from slight impairment of upgaze in adduction of the right eye. The
ILANKOVAN
HEM
421
ET AL
SCREEN CHART FIELD OF RIQHT EVE (fixing with kti eye)
DIAGNOSIS
Green before Left Eye
A HESSSCREENCHART FIELD OF RIGHT EYE (hxmg wth lett eye)
DIAGNOSIS
Green before Lell Eye
Green before Right Eye
B FIGURE 1. Hess screen charts of the patient. A, Limitation of elevation on adduction of the right eye and overaction of the superior rectus of the fellow eye. B, Chart plotted 9 months later showing recovery of function.
forced duction test to elevation in adduction was positive, and a clinical diagnosis of right acquired Brown’s syndrome was made. A Hess screen test (Fig 2) supported the diagnosis. A subconjunctival injection of 4 mg of betamethasone was given and the patient was reexamined 2 months later. He was also advised to exercise his eyes in all directions at regular intervals. A significant improvement in his symptoms of diplopia was noted, and the field
of binocular single vision was central and wide. No further intervention was deemed necessary.
Discussion The superior orbital wall is triangular in shape and comprises the orbital plate of the frontal bone
422
ACQUIRED BROWN’S SYNDROME: IATROGENIC
Nam
HESS SCREEN CHART
CAUSES
11..5..88
1.P.
FIELD OF RIGHT EVE (fcung woth left eye)
Green bsfore Lsft Eye
DIAGNOSIS
HESSSCREEN
CHART
FIELO OF LEFT EVE (fwng wth rnght eve)
DIAGNOSIS
Green before Left Eye
FIELD OF RIGHT EVE (fcmg wtth left eye)
Green before Alght Eye
FIGURE 2. Hess screen charts of the patient. A, Chart plotted 2 weeks following surgery. Clinical assessment reveals a latent convergent squint with slight left hyperphoria in the primary position of gaze. This accounts for the decentration of the two squares. The right eye shows impaired elevation in adduction due to restriction of the superior oblique muscle. B, Chart plotted 9 months later. The impaired elevation in adduction of the right eye is seen only with the outer square.
anteriorly and the lesser wing of the sphenoid bone posteriorly. The trochlea and the fossa for the lacrimal gland constitute two important features of the orbital root. The fovea trochlearis is a small circular dimple superomedially approximately 4.5 mm posterior to the orbital margin. The trochlea, which
may calcify in the elderly, is situated below the fovea trochlearis. The superior oblique muscle takes origin from the annulus of Zinn (Fig 3). It courses anteriorly along the nasal wall of the orbit for approximately 40 mm toward the trochlea. Approximately 9 mm posterior to the trochlea the mus-
ILANKOVAN
423
ET AL
nor rectusmude
irpri
Lateral mctusmuscle
lnfencr
B
Ihlmotmlque
FIGURE 3. the side.
Diagrammatic representation
rem muscle
IruStle
of the relationships of the superior oblique muscle of the eye, A, from above and, B, from
cle becomes tendinous. The tendon within the trochlea turns posteriorly through an angle of 55” and inserts under the superior rectus on the posterior superotemporal quadrant of the globe.” Brown’ postulated that the true congenital form of this disorder was due to shortening of the tendon sheath from the trochlea to its insertion in the globe. Reports exist in the literature for*‘,i3 and againsti this theory. The congenital simulated sheath syndrome appears to be due either to a thickened area in the posterior tendon or to a firm attachment of the posterior sheath to the superior oblique tendon. As the trochlea is situated anterior to the thickened tendon, it interferes with the forward movement of the tendon. The acquired causes include derangement of the anatomy, reattachment of the trochlea at a different site, and healing by possible excess fibrous reaction. These, in turn, can impair free movement of the tendon.i4 In the differential diagnosis, paralysis of the inferior oblique muscle” and, if there is a history of trauma, a blowout fracture of the orbital floor” should be considered. Brown’s syndrome is characterized by depression of the adducted eye, normal action of the contralateral superior rectus muscle, and divergence in upward gaze. These features are not typical of inferior oblique paralysis.3 Furthermore!, a positive forced duction test effectively differentiates between the two disorders.15 Incisions in and around the orbit are not uncommonly performed for trauma, craniofacial deformity, and tumor surgery. The reported cases are ex-
amples of the first two causes. However, the occurrence of this syndrome after surgery is unusual,(j because surgical dissections are performed subperiosteally with little disturbance of the anatomy of the trochlea and the tendon. When the syndrome does occur, it may be frustrating and troublesome. The recommended treatments include muscle exercise, I6 injection of local steroids in the trochlear area,” and surgery to reduce the tethering in the region of the trochlea.” Goldhammer and Smithi reported two cases of acquired Brown’s syndrome, one of which was due to a mild blow leading to periorbital ecchymosis, and the other was of unknown etiology. In both cases radiographs of the skull and orbits were normal, as were the results of neurologic examination. The patients were instructed to exercise their eyes in all direction of gaze every hour for several weeks. Both patients reported marked improvement in their double vision, after 6 months in the first case and 2 weeks in the second. However, muscle exercise as a treatment for this disorder is not well documented in the literature, and we are not aware of any controlled study on the value of exercise. The results of local steroid injection to reduce the tethering caused by scarring in the region of the trochlea are often disappointing.18 However, where inflammation is a major feature, the use of steroids may be beneficial. 19**’Such treatment may be of value in treating early postoperative or posttraumatic cases, presumably by inhibiting fibroblastic
424
ACQUIRED BROWN’S SYNDROME: IATROGENIC
activity in the trochlear
region, as in our second
^^^^
GIST.
Past experience regarding the results of surgery designed to reduce the tethering caused bv scarring in the trochlear region has shown that this procedure is usually unsatisfactory.3 There is a tendency for the operation to cause additional fibrosis.” Brown* in-1973 described a group of 26 patients who were treated surgically; full correction of the motility defect was achieved in only 5, and improvement occurred in 13. In view of these less-than-satisfactory results, and the fact that spontaneous recovery may occur in acquired cases,*l the indications for surgery are restricted. When the field of binocular single vision is wide and comfortable in the primary position of gaze, as in our two cases, surgery is not advocated. On the other hand, if diplopia is experienced in the primary position of gaze, surgery should be considered in an attempt to restore binocular single vision. ** The structure of the trochlea should always be borne in mind while performing exploratory or elective surgical procedures in the region of the superonasal margin of the orbit, and care should be taken not to cause damage. Summary Two cases of iatrogenic acquired Brown’s syndrome are presented, and other causes of this disorder and its treatment are discussed. Care should be taken not to cause damage when operating in the region of the trochlea. Acknowledgment Our sincere thanks to Professor W.H. Reid for allowing us to report case 1.
References 1. Brown HW: Congenital structural muscle anomalies, in Allen JH (ed): Strabismus Ophthalmic Symposium (ed 1) St Louis, MO, Mosby, 1950, pp 205-236
CAUSES
2. Brown HW: True and simulated superior oblique tendon sheath syndrome. Dot Ophthalmol 34:123, 1973 3. Von Noordeen GK: Binocilar Vision and Ocular Motility (ed 3). St Louis, MO, Mosby, 1985, p 380 4. Sandford-Smith JH: Superior oblique tendon sheath syndrome and its relationship to stenosing tenosynovitis. Br J Ophthalmol 57:859, 1973 5. Killian PJ, McClain B, Lawless OH: Brown’s syndrome: An unusual manifestation of rheumatoid arthritis. Arthritis Rheum 20:1080, 1977 6. Blanchard CL, Young LA: Acquired inflammatory superior oblique tendon sheath (Brown’s) syndrome. Arch Otolaryngol 110: 120, 1984 7. Jackson OB, Nankin SJ. Scott WE: Traumatic simulated Brown’s syndrome: A case report. J Ophthalmol Strabismus 16:160, 1979 8. Al-@rainy IA, Dutton GN, Moos KF et al: Orbital injury complicated by entrapment of the superior oblique -tendon: A case report. Br J Oral Maxillofac Surg 26:336, 1988 9. Wesley RE, McCord CD: Tension pneumocephalus from orbital roof fracture. Ann Ophthalmol 14: 184, 1982 10. Booth-Mason S. Kyle GM, Rosser M, et al: Acquired Brown’s syndrome: An unusual cause. Br J Ophthalmol 69:791, 1985 11. Parks MM: The superior oblique tendon. Trans Ophthalmol Sot UK 97:288, 1977 12. Folk ER: Superior oblique tendon sheath syndrome. Arch Ophthalmol 57:39, 1957 13. Esterly MD. Nadpath RP, Russell JS: Tendon sheath syndrome. Arch Ophthalmol 63:997. 1960 14. Parks MM, Brown M: Superior oblique tendon sheath syndrome of Brown. Am J Ophthalmol 79:82, 1975 15. Zipf RF, Trokel SL: Simulated superior oblique tendon sheath syndrome following orbital floor fracture. Am J Ophthalmol 75:700, 1973 16. Goldhammer Y, Smith JL: Acquired intermittent Brown’s syndrome. Neurology 24:666, 1974 17. Hermann JS: Acquired Brown’s syndrome of inflammatory origin. Arch Ophthalmol 96:1228, 1978 18. Mein J, Harcourt B: Diagnosis and Management of Ocular Motilitv Disorders (ed 1). Oxford, London. Blackwell Scientific,.1986, p 304 19. Trimble RB. Kelly V, Mitchell M: Acquired Brown’s syndrome, in Ravault AP, Lenk M (eds): Transactions of the International Orthoptic Congress, Lyons, France, LIPS, 1982, pp 267-273 20. Roper-Hall MJ. Roper-Hall G: Orthoptics. Proceedings of the Second International Orthoptic Congress. Excerpta Medica, 1972. pp 360-366 21. Lowe RF: Bilateral superior oblique tendon sheath syndrome. Occurrence and spontaneous recovery in one of uniovular twins. Br J Ophthalmol 53:466, 1969 22. Waddell E: Brown’s syndrome revisited. Br Orthopt J 39: 17. 1982
J Oral Maxdlofac
ACQUIRED BROWN’S SYNDROME: IATROGENIC CAUSES
Surg
40:42@424,1990
Acquired Brown’s Syndrome: la trogenic Causes V. ILANKOVAN, FDSRCS, FRCS(ED),* LA. AL-QURAINY, MB, CHB, MCOPHTH, DO,t K.F. MOOS, FDSRCS, FRCS(ED),$- AND G.N. DUTTON, MD, FRCS§
Brown’s syndrome, or superior oblique tendon sheath syndrome, is a restrictive ocular motility disorder in which there is impairment of free movement of the tendon of this muscle through the trochlea. It was described in 1950 by Brown,’ who later classified it into true and simulated forms.’ The former is always due to a congenital cause, whereas the simulated form can be either congenital or acquired.* The disorder is characterised by restriction of elevation of the eye on adduction associated with a positive forced duction test in that direction. Elevation in the primary position of gaze is normal or near normal. Other features include widening of the palpebral fissure on adduction and, occasionally, minimal overaction of the ipsilateral superior oblique muscle.3 Many acquired causes have been described in the literature. Stenosing tenosynovitis,4 rheumatoid arthritis,’ and adjacent sinusitis6 comprise inflammatory causes, whereas injury’.* and surgical blepharoplasty’ have been implicated as traumatic causes. Metastatic deposits may also give rise to this condition.” We report two cases in which surgical procedures in the region of the trochlea have resulted in Brown’s syndrome.
Received from Canniesburn Hospital, Bearsden, Glasgow, UK; and Tennent Institute of Ophthalmology, Western Infirmary, Glasgow, UK. * Reeistrar in Oral and Maxillofacial Surgerv. _ _ t Research Fellow. $ Consultant in Oral and Maxillofacial Surgery. § Consultant in Ophthalmology. Address correspondence and reprint requests to Mr Ilankovan: Department of Oral and Maxillofacial Surgery, Canniesburn Hospital, Bearsden, Glasgow G61 IQL, UK. 0 1990 American
Association
geons 0278-2391/90/4804-0018$3.00/0
of Oral and Maxillofacial
Sur-
Report of Two Cases Case 1 A 22-year-old woman was involved in a traffic accident in November 1982; she sustained lacerations to both her upper eyelids and supraorbital regions. The wounds were repaired in the casualty department. Since then, two further plastic surgical procedures have been carried out to revise the scars and to remove fragments of glass from the left supraorbital region. The patient did not initially have any visual symptoms. However, early in 1988, an infection around the right medial canthal region raised the suspicion of a retained foreign body. The area was explored, but no foreign body was found. When the patient was subsequently reexamined, she complained of double vision and difficulty in focusing. An ophthalmic opinion was sought. Examination revealed impairment of elevation of the right eye on adduction associated with diplopia. The forced duction test in the direction of impairment was positive. Hess screen charts (Fig 1) supported this finding, and a diagnosis of acquired Brown’s syndrome was made. This was thought to be due to scarring around the right trochlea following the exploratory surgery, which had prevented free movement of the superior oblique tendon through the trochlea. No treatment was carried out because the field of binocular single vision was wide and central.
Case 2 A 21-year-old man with congenital hypertelorism underwent various subcranial surgical procedures between 1980 and 1988. The most recent operation involved bilateral malar osteotomies with bone grafting via a bicoronal flap. Within a week after the operation the patient complained of double vision for the first time. Radiographs failed to show any abnormality. An ophthalmic opinion was sought, and examination revealed unaided visual acuities of 20/16.7 for each eye. In slight depression he had no double vision, but there was a demonstrable latent divergence and a slight left hyperphoria. This broke down into a vertical squint with divergence on upgaze to the left, requiring a 3-diopter base-up prism before the left eye to correct the diplopia. This indicated that the patient had an antecendent esophoria which became an esotropia on elevation due to loss of fusion resulting from slight impairment of upgaze in adduction of the right eye. The
ILANKOVAN
HEM
421
ET AL
SCREEN CHART FIELD OF RIQHT EVE (fixing with kti eye)
DIAGNOSIS
Green before Left Eye
A HESSSCREENCHART FIELD OF RIGHT EYE (hxmg wth lett eye)
DIAGNOSIS
Green before Lell Eye
Green before Right Eye
B FIGURE 1. Hess screen charts of the patient. A, Limitation of elevation on adduction of the right eye and overaction of the superior rectus of the fellow eye. B, Chart plotted 9 months later showing recovery of function.
forced duction test to elevation in adduction was positive, and a clinical diagnosis of right acquired Brown’s syndrome was made. A Hess screen test (Fig 2) supported the diagnosis. A subconjunctival injection of 4 mg of betamethasone was given and the patient was reexamined 2 months later. He was also advised to exercise his eyes in all directions at regular intervals. A significant improvement in his symptoms of diplopia was noted, and the field
of binocular single vision was central and wide. No further intervention was deemed necessary.
Discussion The superior orbital wall is triangular in shape and comprises the orbital plate of the frontal bone
422
ACQUIRED BROWN’S SYNDROME: IATROGENIC
Nam
HESS SCREEN CHART
CAUSES
11..5..88
1.P.
FIELD OF RIGHT EVE (fcung woth left eye)
Green bsfore Lsft Eye
DIAGNOSIS
HESSSCREEN
CHART
FIELO OF LEFT EVE (fwng wth rnght eve)
DIAGNOSIS
Green before Left Eye
FIELD OF RIGHT EVE (fcmg wtth left eye)
Green before Alght Eye
FIGURE 2. Hess screen charts of the patient. A, Chart plotted 2 weeks following surgery. Clinical assessment reveals a latent convergent squint with slight left hyperphoria in the primary position of gaze. This accounts for the decentration of the two squares. The right eye shows impaired elevation in adduction due to restriction of the superior oblique muscle. B, Chart plotted 9 months later. The impaired elevation in adduction of the right eye is seen only with the outer square.
anteriorly and the lesser wing of the sphenoid bone posteriorly. The trochlea and the fossa for the lacrimal gland constitute two important features of the orbital root. The fovea trochlearis is a small circular dimple superomedially approximately 4.5 mm posterior to the orbital margin. The trochlea, which
may calcify in the elderly, is situated below the fovea trochlearis. The superior oblique muscle takes origin from the annulus of Zinn (Fig 3). It courses anteriorly along the nasal wall of the orbit for approximately 40 mm toward the trochlea. Approximately 9 mm posterior to the trochlea the mus-
ILANKOVAN
423
ET AL
nor rectusmude
irpri
Lateral mctusmuscle
lnfencr
B
Ihlmotmlque
FIGURE 3. the side.
Diagrammatic representation
rem muscle
IruStle
of the relationships of the superior oblique muscle of the eye, A, from above and, B, from
cle becomes tendinous. The tendon within the trochlea turns posteriorly through an angle of 55” and inserts under the superior rectus on the posterior superotemporal quadrant of the globe.” Brown’ postulated that the true congenital form of this disorder was due to shortening of the tendon sheath from the trochlea to its insertion in the globe. Reports exist in the literature for*‘,i3 and againsti this theory. The congenital simulated sheath syndrome appears to be due either to a thickened area in the posterior tendon or to a firm attachment of the posterior sheath to the superior oblique tendon. As the trochlea is situated anterior to the thickened tendon, it interferes with the forward movement of the tendon. The acquired causes include derangement of the anatomy, reattachment of the trochlea at a different site, and healing by possible excess fibrous reaction. These, in turn, can impair free movement of the tendon.i4 In the differential diagnosis, paralysis of the inferior oblique muscle” and, if there is a history of trauma, a blowout fracture of the orbital floor” should be considered. Brown’s syndrome is characterized by depression of the adducted eye, normal action of the contralateral superior rectus muscle, and divergence in upward gaze. These features are not typical of inferior oblique paralysis.3 Furthermore!, a positive forced duction test effectively differentiates between the two disorders.15 Incisions in and around the orbit are not uncommonly performed for trauma, craniofacial deformity, and tumor surgery. The reported cases are ex-
amples of the first two causes. However, the occurrence of this syndrome after surgery is unusual,(j because surgical dissections are performed subperiosteally with little disturbance of the anatomy of the trochlea and the tendon. When the syndrome does occur, it may be frustrating and troublesome. The recommended treatments include muscle exercise, I6 injection of local steroids in the trochlear area,” and surgery to reduce the tethering in the region of the trochlea.” Goldhammer and Smithi reported two cases of acquired Brown’s syndrome, one of which was due to a mild blow leading to periorbital ecchymosis, and the other was of unknown etiology. In both cases radiographs of the skull and orbits were normal, as were the results of neurologic examination. The patients were instructed to exercise their eyes in all direction of gaze every hour for several weeks. Both patients reported marked improvement in their double vision, after 6 months in the first case and 2 weeks in the second. However, muscle exercise as a treatment for this disorder is not well documented in the literature, and we are not aware of any controlled study on the value of exercise. The results of local steroid injection to reduce the tethering caused by scarring in the region of the trochlea are often disappointing.18 However, where inflammation is a major feature, the use of steroids may be beneficial. 19**’Such treatment may be of value in treating early postoperative or posttraumatic cases, presumably by inhibiting fibroblastic
424
ACQUIRED BROWN’S SYNDROME: IATROGENIC
activity in the trochlear
region, as in our second
^^^^
GIST.
Past experience regarding the results of surgery designed to reduce the tethering caused bv scarring in the trochlear region has shown that this procedure is usually unsatisfactory.3 There is a tendency for the operation to cause additional fibrosis.” Brown* in-1973 described a group of 26 patients who were treated surgically; full correction of the motility defect was achieved in only 5, and improvement occurred in 13. In view of these less-than-satisfactory results, and the fact that spontaneous recovery may occur in acquired cases,*l the indications for surgery are restricted. When the field of binocular single vision is wide and comfortable in the primary position of gaze, as in our two cases, surgery is not advocated. On the other hand, if diplopia is experienced in the primary position of gaze, surgery should be considered in an attempt to restore binocular single vision. ** The structure of the trochlea should always be borne in mind while performing exploratory or elective surgical procedures in the region of the superonasal margin of the orbit, and care should be taken not to cause damage. Summary Two cases of iatrogenic acquired Brown’s syndrome are presented, and other causes of this disorder and its treatment are discussed. Care should be taken not to cause damage when operating in the region of the trochlea. Acknowledgment Our sincere thanks to Professor W.H. Reid for allowing us to report case 1.
References 1. Brown HW: Congenital structural muscle anomalies, in Allen JH (ed): Strabismus Ophthalmic Symposium (ed 1) St Louis, MO, Mosby, 1950, pp 205-236
CAUSES
2. Brown HW: True and simulated superior oblique tendon sheath syndrome. Dot Ophthalmol 34:123, 1973 3. Von Noordeen GK: Binocilar Vision and Ocular Motility (ed 3). St Louis, MO, Mosby, 1985, p 380 4. Sandford-Smith JH: Superior oblique tendon sheath syndrome and its relationship to stenosing tenosynovitis. Br J Ophthalmol 57:859, 1973 5. Killian PJ, McClain B, Lawless OH: Brown’s syndrome: An unusual manifestation of rheumatoid arthritis. Arthritis Rheum 20:1080, 1977 6. Blanchard CL, Young LA: Acquired inflammatory superior oblique tendon sheath (Brown’s) syndrome. Arch Otolaryngol 110: 120, 1984 7. Jackson OB, Nankin SJ. Scott WE: Traumatic simulated Brown’s syndrome: A case report. J Ophthalmol Strabismus 16:160, 1979 8. Al-@rainy IA, Dutton GN, Moos KF et al: Orbital injury complicated by entrapment of the superior oblique -tendon: A case report. Br J Oral Maxillofac Surg 26:336, 1988 9. Wesley RE, McCord CD: Tension pneumocephalus from orbital roof fracture. Ann Ophthalmol 14: 184, 1982 10. Booth-Mason S. Kyle GM, Rosser M, et al: Acquired Brown’s syndrome: An unusual cause. Br J Ophthalmol 69:791, 1985 11. Parks MM: The superior oblique tendon. Trans Ophthalmol Sot UK 97:288, 1977 12. Folk ER: Superior oblique tendon sheath syndrome. Arch Ophthalmol 57:39, 1957 13. Esterly MD. Nadpath RP, Russell JS: Tendon sheath syndrome. Arch Ophthalmol 63:997. 1960 14. Parks MM, Brown M: Superior oblique tendon sheath syndrome of Brown. Am J Ophthalmol 79:82, 1975 15. Zipf RF, Trokel SL: Simulated superior oblique tendon sheath syndrome following orbital floor fracture. Am J Ophthalmol 75:700, 1973 16. Goldhammer Y, Smith JL: Acquired intermittent Brown’s syndrome. Neurology 24:666, 1974 17. Hermann JS: Acquired Brown’s syndrome of inflammatory origin. Arch Ophthalmol 96:1228, 1978 18. Mein J, Harcourt B: Diagnosis and Management of Ocular Motilitv Disorders (ed 1). Oxford, London. Blackwell Scientific,.1986, p 304 19. Trimble RB. Kelly V, Mitchell M: Acquired Brown’s syndrome, in Ravault AP, Lenk M (eds): Transactions of the International Orthoptic Congress, Lyons, France, LIPS, 1982, pp 267-273 20. Roper-Hall MJ. Roper-Hall G: Orthoptics. Proceedings of the Second International Orthoptic Congress. Excerpta Medica, 1972. pp 360-366 21. Lowe RF: Bilateral superior oblique tendon sheath syndrome. Occurrence and spontaneous recovery in one of uniovular twins. Br J Ophthalmol 53:466, 1969 22. Waddell E: Brown’s syndrome revisited. Br Orthopt J 39: 17. 1982
