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In a 20-year-old man with a history of sinonasal polyps, bilateral ophthalmoplegia, exophthalmos, and optic nerve dysfunction developed. Radiologic imaging showed a polypoid mass filling the nose and sinuses, eroding into the pituitary fossa, basal cisterns, and orbits, and compressing the cavernous sinuses. Six months after bilateral maxillary, ethmoid, and sphenoid exploration, ocular motility returned to normal, but there remained mild generalized visual field loss in the right eye. The pathologic specimen showed polypoid respiratory mucosa with acute and chronic inflammation as well as eosinophiles.

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Necrotizing scleritis with inflammation of the right eye developed after bilateral eye muscle surgery for thyroid ophthalmopathy. Debilitating pain, delay in onset, and involvement of the sclera distinguish this condition from anterior segment ischemia. The surgery may have acted as a nonspecific trigger in an eye at risk for scleritis. Necrotizing scleritis has occurred infrequently after other types of eye surgery but, to our knowledge, has not been previously reported as a complication of eye muscle surgery.

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Three patients with simulated Brown's superior oblique tendon sheath syndrome are presented. With the use of computed tomographic (CT) findings, the site of the pathology could be demonstrated. In all three patients, there were definite abnormal findings in the anterior sheath of the reflected tendon of the superior oblique. The abnormal findings in one case were confirmed at the time of surgery. Therapy in two of the cases was determined by the abnormal findings on the CT scan.

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Four cases of isolated inferior rectus transection secondary to trauma are presented. The clinical and CT scan findings are illustrated. The CT scan findings are very useful in the surgical management and prognosis of these cases.

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Computed tomographic (CT) findings in 4 patients with superior oblique tendon sheath syndrome (congenital or acquired Brown syndrome) are described. When the inferior oblique muscle moves the eye upward, the superior oblique muscle normally relaxes, while its tendon lengthens and slides freely through the trochlea. In Brown syndrome this process is somehow restricted, which is most apparent during attempts at elevation when the eye is adducted, resulting in an apparent inferior oblique "palsy" (pseudopalsy). Brown syndrome is the most common cause of an apparent isolated limitation of the inferior oblique muscle. CT is a valuable tool in understanding the pathophysiology and management of acquired Brown syndrome, showing thickening and inflammatory changes of the reflected portion of the superior oblique tendon.

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We studied 250 patients with consecutive exotropia. The interval between the surgical procedure and the onset of the consecutive exotropia may take many years. Consecutive exotropia occurred with all types of corrective esotropia surgery that we studied. Amblyopia and medial rectus limitation postoperatively seemed to be common factors associated with consecutive exotropia.

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We detected mild afferent pupillary defects with the "swinging flashlight" test in 4 out of 45 amblyopic patients. Our study was designed to minimize the effect of observer bias and to control for the difficulty of testing the pupils in young children. We found afferent defects in both strabismic and anisometropic amblyopes. There was no apparent relationship between pupillary response and visual acuity: afferent defects were noted in association with better than 20/100 vision in three cases but were absent in a majority of patients with profound visual loss. Vision was improved by occlusion therapy in two amblyopes with pupillary abnormalities. We regard the occurrence of afferent pupillary defects as evidence for a physiological disturbance at the retinal level in at least some cases of amblyopia. Our findings suggest that the extent of retinal involvement in amblyopic eyes is independent of reduction in acuity, to which primary cortical abnormalities may contribute as well.

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Two patients were treated for a previously unreported disorder believed to be related to Marcus Gunn jaw-winking. The first, a 9-month-old infant with left congenital blepharoptosis without jaw-winking and with normal ocular motility had an up and down movement of the left globe synchronous with nursing movements of the jaw. The second was a 5-year-old girl with left blepharoptosis, jaw-winking, and left double elevator palsy who had up and down movements of both the left upper lid and the left globe synchronous with chewing. The left globe movements were most prominent in the field of vertical action of the superior rectus muscle and persisted after levator excision and fascia lata sling procedures. The possible etiology of the Marcus Gunn jaw-winking phenomenon is discussed and related to our cases of eye bobbing. The eye bobbing probably is caused by abnormal innervation to the superior rectus muscle produced by jaw movements in a manner analogous to the abnormal stimulation of the levator muscle in jaw-winking. The similar embryologic development and innervation of the levator and superior rectus muscles add credence to this theory.

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A patient with classical Apert's syndrome is discussed along with the finding of absent superior rectus muscle. This anomaly may be more common than thought, especially in relation to craniofacial anomalies. A review of Apert's syndrome and superior rectus agenesis is presented.

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We studied eye position under general anesthesia in 51 patients with concomitant esotropia or exotropia, divided into two groups. One group consisted of strabismus patients who had had no previous surgery. The second group consisted of strabismus patients who had undergone previous surgery on one (asymmetric) or both (symmetric) eyes. We found that both groups showed either no change or more divergence under general anesthesia in comparison to their preoperative state. Those patients who had had no previous surgery revealed an equal divergence in both eyes. This relationship also held true for those patients who had undergone symmetrical surgery in both eyes. However, those patients who had had surgery in one eye only showed more divergence in the operated eye than in the unoperated one. These findings reflect the mechanical--anatomical factors created by the surgery itself.

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The medical records of 33 consecutive patients who developed secondary exotropia following surgery for esotropia were reviewed. Only six patients (18%) had normal medial rectus function. Lateral rectus recession proved to be an excellent procudure for correcting the deviation in these patients, provided the surgery was limited to the eye with the narrower palpebral fissure. Twenty-seven patients (82%) exhibited limitation of adduction secondary to medial rectus underaction. Of these patients, 75% were successfully corrected following a 12 mm advancement and resection of the underacting medial rectus muscle. The details of the surgical technique performed are discussed.

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Nineteen patients with residual esotropia following conventional maximum horizontal recess-resect surgery were treated by further recession of the medial rectus muscle to a point 13.5 mm from the limbus. Six of these patients also underwent an 8-mm resection of the ipsilateral lateral rectus in addition to the medial recession. Eighteen of the patients achieved a good to excellent cosmetic result in the primary position. One patient was markedly overcorrected probably secondary to an unwarranted lateral rectus resection. Most of the patients showed some mild limitation of adduction, but this was generally not a significant cosmetic or functional defect. The degree of limitation seen was no greater than that which has been observed in similar patients treated by marginal myotomy. Recession of the medial rectus muscle 13.5 mm from the limbus seems to be a safe and effective method of treating surgically undercorrected esotropia.

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