Elevation In Adduction Research Articles

Congenital Oculomotor Nerve Synkinesis Associated Wwith Fetal Retinoid Syndrome

Isotretinoin (RA), used for the treatment of cystic acne, is a powerful teratogen, causing craniofacial dysmorphisms and neural tube defects. We present two patients with RA embryopathy and oculomotor nerve synkinesis. Retrospective review of patient records. Two patients presented with third nerve synkinesis and fetal RA exposure. Both had marked elevation of the upper eyelids on adduction such that the lid fissures alternately opened and closed on gaze from side to side. Both patients showed typical dysmorphisms of RA embryopathy. The first patient had complete agenesis of the cerebellar vermix and died at 2 years. The second patient had restricted extraocular muscles in one eye and was exotropic and hypotropic. Both patients demonstrated simultaneous innervation of the medial rectus and levator palpebrae muscles causing coincident lid elevation in adduction. This evidence of oculomotor nerve synkinesis is consistent with animal studies showing abnormalities in the formation of cranial nerve ganglia following fetal RA exposure. RA is a powerful teratogen. These patients provide additional clinical evidence of its influence on neural migration during early development.

Nasal myectomy of the inferior oblique muscles for recurrent elevation in adduction

Recurrence of inferior oblique overaction (IOOA) after recession or anterior transposition of the inferior oblique (IO) muscles is a common problem. We have been treating such cases by nasal myectomy of the IO, where a segment of approximately 5 mm is removed from the nasal portion, leaving the temporal portion of the IO with its insertion and its ancillary origin, the neurofibrovascular junction, intact. Here we report long-term findings on this procedure. Records were analyzed on 72 eyes belonging to 40 patients with recurrent IOOA of grade +1 or more, who received nasal myectomy of the inferior oblique (NMIO) in one (8 cases) or both (32 cases) eyes, and who had a minimum of 3 months follow-up. At follow-up (range 3.6 months to 12 years; median 26 months), 27 patients (68%) showed no IO overaction, whereas 11 (28%) showed improvement of at least one grade point and 2 (5%) showed no improvement. Of the patients with residual IO overaction, three received additional surgery: in two of these patients IO overaction was subsequently eliminated while no additional follow-up was available for the third patient. The effects of NMIO on dissociated vertical deviation were variable. In 95% of these patients nasal myectomy of the IO resulted in reduction and in many cases elimination of IO overaction. An advantage of this procedure is that the temporal portion of the muscle, with its ancillary origin and insertion, is preserved.

Unilateral anterior transposition of the inferior oblique muscle for correction of hypertropia in primary position

Purpose To evaluate the correction of hypertropia in primary position with unilateral inferior oblique (IO) anterior transposition (IOAT). Methods Ten patients with idiopathic (nonparalytic, restrictive, or dissociated vertical deviation) hypertropia with marked IO overaction, who underwent unilateral IOAT, were prospectively evaluated to observe the correction of the hypertropia in primary position. No previous ocular muscle surgery had been performed. Four patients had esotropia and two had exotropia. In addition to the proposed surgery, horizontal procedures were performed to correct horizontal deviation, but no vertical transposition of horizontal muscles was done. Four patients had hypertropia and IO overaction, without horizontal strabismus, and IOAT was the only procedure performed. The IO muscle was reinserted 1 mm laterally to the lateral extremity of the inferior rectus muscle insertion using only one suture. The statistical analysis was performed by Wilcoxon rank sum test. Results The mean absolute correction in primary position was 18.1 prism diopters (PD) (range, 4 to 33), directly proportional to the size of the hypertropia before surgery. Nine of the 10 patients had a residual vertical deviation of ≤6 PD. After surgery, 4 patients (40%) presented limited elevation in adduction (−2) in the field of the operated IO, presumably caused by the antielevator effect of the transposed muscle, which did not improve during the follow-up period (range, 2 to 79 months). Conclusion Unilateral IOAT is an effective technique for correction of large hypertropia associated with marked unilateral IO overaction. Some lower lid curvature deformity and some limitation of elevation were observed in forced upgaze in some patients, but this was of no cosmetic importance.

Large-segment superior oblique tendon expanders in the management of severe congenital brown syndrome

Purpose To report the effectiveness of large-segment superior oblique tendon expanders for severe congenital Brown syndrome. Methods Medical records of 12 consecutive patients with severe congenital Brown syndrome were evaluated retrospectively. All patients had a hypotropia > 20 prism diopters in primary position. A superior oblique tendon lengthening procedure, using a 10- to 12-mm—long silicone band, was performed on each patient. Preoperative and postoperative extraocular motility patterns were analyzed, and the final results were graded as “excellent,” “good,” “fair,” “poor, undercorrected” and “poor, overcorrected.” Results As of the last recorded follow-up examination (mean, 32 months), three patients had an excellent result, six had a good result, three had a fair result, and none had a poor result. All patients experienced an improvement in their severe Brown syndrome, with 100% showing a postoperative primary-position hypotropia < 8 prism diopters. Postoperative limitation of elevation in adduction was either −1 or −2 for all patients. No patient required further surgery, and no extrusions of the implants were noted. Conclusion The superior oblique tendon expander procedure appears to be an effective tool in the surgical treatment of severe Brown syndrome. The use of a large-segment (10- to 12-mm) band seems to be an appropriate choice when dealing with patients having primary-position hypotropia > 20 prism diopters.

Anterior and nasal transposition of the inferior oblique muscles

Background When performing anterior transposition of the inferior oblique (IO) muscle, placement of the posterior suture close to the lateral border of insertion of the inferior rectus (IR) muscle decreases the incidence of antielevation syndrome (AES). We hypothesized that placement of the suture nasal to the IR muscle insertion will convert the IO muscle into an intorter and depressor. Here we present the first series of results obtained with a new procedure for the treatment of elevation in adduction with extorsion and abnormal head postures. Methods Twenty patients with IO muscle overaction, superior oblique (SO) muscle palsy, absent SO muscles, AES, or Duane syndrome were studied. Before surgery, each patient showed at least one, but often more, of the following signs: elevation in adduction, exotropia (XT) in up gaze, abnormal head posture, and extorsion. Each underwent anterior and nasal transposition (ANT) of the IO muscle, with the new insertion typically 2 mm nasal and 2 mm posterior to the nasal border of the IR muscle insertion. Results Large improvements in ocular alignment, extorsion, and head posture were found in most patients. However, a poor result was noted in a patient with Y-pattern XT, who developed a mild amount of comitant XT after an extreme degree of ANT (4 mm nasal and 3 mm anterior to the nasal border of the IR muscle insertion). In Duane syndrome, ANT corrects upshoot, but downshoot may get worse. Mersilene permanent sutures, rather than dissolving suture materials, are recommended to avoid postoperative retraction of muscle fibers. Conclusions ANT converts the IO muscle into an intorter and tonic depressor and can significantly improve elevation in adduction. This procedure seems particularly useful in patients with severe or recurrent congenital and acquired SO palsies, particularly as a secondary procedure. Extreme ANT may induce exotropia in the primary position.

Magnetic resonance imaging of the functional anatomy of the inferior oblique muscle in superior oblique palsy

Purpose To study size and contractility of the normal inferior oblique (IO) muscle using high-resolution magnetic resonance imaging (MRI) and to evaluate abnormalities of the superior oblique (SO) and IO muscles in chronic SO palsy. Design Prospective, case control study. Participants Thirteen patients with SO palsy and 17 orthotropic subjects. Methods High-resolution, surface coil MRI was used to obtain sets of contiguous, 2-mm thick coronal and sagittal images repeated in multiple gaze directions. Digital image analysis was used to measure IO and SO muscle cross-sectional areas for evaluation of size and contractility. Diagnosis of SO palsy in one bilateral and 12 unilateral cases was based on subnormal contractility and SO size less than the normal 95% confidence limit. Ipsilesional and contralesional oblique muscles were compared with controls and correlated with clinical characteristics. Results In all subjects, anterior movement and contractile thickening of the IO were observed in supraduction, with posterior movement and relaxational thinning in infraduction. The mean (± standard deviation) cross-sectional area of 15 normal control IO muscles was 13.4 ± 3.9 mm 2, with mean contractile increase from infraduction to supraduction of 5.7 ± 2.6 mm 2. Subjects with SO palsy had incomitant hypertropia with a wide range of overelevation and underelevation in adduction (i.e., upshoot, downshoot). SO atrophy correlated with underdepression in adduction ( P < 0.0001). Contralesional SO cross-section was slightly greater than normal ( P = 0.004). The IO cross-section ipsilesional and contralesional to SO palsy did not, however, differ significantly from normal and did not correlate with elevation in adduction ( P > 0.2). Conclusions Quantitative morphometry by MRI can demonstrate IO size and contractility. Even in cases of unequivocal SO palsy associated with ipsilesional SO atrophy and deficient contractility, the degree of elevation in adduction was not correlated with IO size. This finding suggests that the associated overelevation in adduction, commonly termed “inferior oblique overaction,” actually arises from some other mechanism than IO hypertrophy or excess contractility. Revision of clinical terminology seems warranted.

An adjustable superior oblique tendon spacer with the use of nonabsorbable suture

Purpose: Philip Knapp described a method, sometimes referred to as the “chicken suture,”of securing a loose nonabsorbable suture to the cut ends of the superior oblique tendon to facilitate future reversal. The purpose of this study is to describe a modification of Knapp's technique to achieve partial, reversible, and intraoperatively adjustable superior oblique weakening. Methods: The superior oblique tendon was exposed, 2 polyester nonabsorbable sutures were placed 4 mm apart, and the tendon was cut. With the use of a slip knot, the cut ends of the tendon were separated by 2 to 8 mm. Tendon separation was adjusted intraoperatively according to the exaggerated traction test and, in some cases, fundus torsion. Medical records of all patients who underwent surgery with this technique were reviewed and the outcomes tabulated. Results: Twelve patients (16 eyes) were treated for superior oblique overaction and 3 patients (3 eyes) for Brown syndrome. Follow-up was 2 to 46 months (mean, 17 months). Mean superior oblique overaction improved from +1.3 before surgery to +0.3 after surgery, mean A pattern improved from 20 PD to 2 PD, and fundus intorsion improved from +1.2 to +0.3. In Brown syndrome, the mean elevation in adduction improved from −3.8 to −1.0. One patient from each group developed an overcorrection. None of the patients developed recurrence. The patients with Brown syndrome continued to improve over a 1-year period. Conclusions: The superior oblique tendon suture spacer is effective, intraoperatively adjustable, and technically easier to perform than a silicone expander procedure. This technique should be considered as an alternative for patients requiring superior oblique weakening. (J AAPOS 2001;5:164-71)

Magnetic resonance imaging features of two cases of acquired Brown's syndrome

The action of the superior oblique muscle depends on both the contractile function of the muscle belly as well as the force transmission function of the tendon trochlea complex. Brown's syndrome is a restriction to elevation in adduction presumed due to an anomaly of the superior oblique tendon trochlea complex. This report presents two patients with an unusual restriction to elevation in adduction in the affected eye, and a clinical picture consistent with a Brown's syndrome. A non-invasive analysis of the functional anatomy of the superior oblique was performed using a high-resolution MRI with surface coils. Imaging in the first case revealed a cyst in the area of the right superior oblique tendon just posterior to the trochlea in primary position. The second patient had undergone reattachment of an avulsed trochlea after a dog bite (canine tooth syndrome). Imaging in the second case revealed scarring and connective tissue disruption around the tendon impeding muscle function. These findings provide distinct mechanical explanations for Brown's syndrome.

The effect of anterior transposition of the inferior oblique muscle on ocular torsion

Introduction: The effects of anterior transposition of the inferior oblique on elevation in adduction have been studied, but changes in objective ocular torsion have not been investigated. Methods: A prospective study on the effect of anterior transposition of the inferior oblique on objective torsion with use of fundus photography was undertaken in 24 eyes of 13 patients. The amount of ocular torsion was determined by measuring the angle formed by a horizontal line drawn across the geometric center of the disc and a second line connecting the geometric center to the foveola. Results: The decrease in excyclotorsion at 6 to 8 weeks after surgery was 6.9 ± 5.0 degrees (34%) ( p = 0.006) and 2.8 ± 4.4 degrees (13%) (not significant) after 10 weeks. An overall net change of 6.2 ± 4.8 degrees (33%) was obtained after anterior transposition of the inferior oblique adjacent or anterior to the inferior rectus insertion ( p = 0.006). Transpositions done 1 to 3 mm behind the inferior rectus insertion showed a negligible torsional change. Torsion where inferior oblique function normalized after anterior transposition of the inferior oblique (8.5 ± 2.9 degrees) was not different from control, whereas torsion where inferior oblique function recurred after surgery (15.9 ± 7.2) was significantly different from control ( p = 0.002). Regression analysis showed that only preoperative inferior oblique overaction and preoperative degree of torsion predicted the change in torsion after anterior transposition of the inferior oblique. Conclusion: Anterior transposition of the inferior oblique muscle initially decreased objective excyclotorsion, but the effect decayed beyond 10 weeks. At least in the short term only anterior transposition of the inferior oblique muscle done adjacent or anterior to the inferior rectus insertion affected torsion.

Brown's syndrome secondary to sinus surgery

Brown's syndrome is characterized by limitation of elevation in adduction along with a positive forced duction test. Acquired cases can be caused by local inflammatory conditions or may be secondary to systemic problems. This report presents the clinical description and management of a patient who developed Brown's syndrome after sinus surgery. A discussion follows describing the specific clinical presentations, etiologies, differential diagnoses, and management of this disorder.

Reversed Fixation Test as a Means to Differentiate between Dissociated and Non-Dissociated Strabismus

Dissociated vertical deviation (DVD) depends on the balance of visual inputs coming through the right and left eyes. In the classical Bielschowsky Filter Test the balance of visual inputs is altered by darkening the retinal image of the fixing eye with a filter. In the Reversed Fixation Test (RFT) the balance of visual inputs is altered by not only darkening the fixing eye (occlusion put on) but also by brightening the squinting eye (occlusion removed) and, at the same time, switching the fixation to the other eye. In a series of 30 patients the RFT revealed a DVD component of 16.3 ± 4.9± while the Bielschowsky Filter Test revealed 3.4 ± 3.2± only. In seven cases the value of the Bielschowsky Filter Test was even zero while the RFT revealed a DVD component between 8 and 20±. The RFT allows a quantitative differentiation between DVD and esotropia with elevation in adduction (= upshoot in adduction or strabismus sursoadductorius or overaction of the inferior oblique muscle), even if both types of vertical deviation occur in the same patient.

Pure anteropositioning of inferior oblique

Anteropositioning of inferior oblique is of late becoming popular but it inadvertently also entails a compulsory recession which may be undesirable at times. We have evaluated the effect of a 'pure' anteropositioning procedure (11 eyes), with Elliot & Nankin's anteropositioning (10 eyes) and Parks' recession (17 eyes). The mean change of vertical deviation in elevation in adduction (surso adduction) was 15.09 +/- 8.3 prism dioptres (p.d.) in pure anteropositioning; 23.50 +/- 5.6 p.d. in E & N's anteropositioning and 14.82 +/- 5.9 p.d. in Parks' recession, showing this procedure to be as effective as a conventional recession procedure. However, while the latter two methods produced an intorsion, 'pure' anteropositioning produced no significant change in torsion. It is a much simpler procedure to weaken the elevation without affecting the torsion.

Spontaneous consecutive Brown syndrome following superior oblique palsy

A 28-year-old female presented with a left trochlear nerve palsy, after indirect head trauma, with no fracture or orbital lesion. She had diplopia, a hypertropia and excyclotropia on right downgaze. Three months later the trochlear palsy had been replaced by Brown's syndrome: a deficit of elevation in adduction, with diplopia, incyclotropia and hypertropia in up-gaze. The Brown syndrome remained the same over a period of 18 months. A 31-year-old male suffered from severe brain contusion with intracerebral haemorrhage and bilateral trochlear nerve palsy. Three years later, he had a bilateral trochlear palsy with bilateral severe Brown's syndrome, with a right hypertropia and 10° to 25° incyclotropia in upgaze and 5° to 10° excyclotropia in downgaze. The field of binocular vision was shifted to left gaze. Orbital CT scan was normal. At surgery, the forced duction test was positive for Brown's syndrome on both sides and the tendon of the superior oblique muscle of the right eye was thickened. The field of binocular vision was centralized after surgery but torsional diplopia in upgaze and downgaze was present as before. Secondary Brown's syndrome after (persisting or vanishing) trochlear nerve palsy without any direct trauma to the superior oblique muscles or the orbit could be caused by a fibrotic reaction of the superior oblique tendon or adjacent structures. This could be due to inactivity or to indirect trauma.

Simultaneous Superior Oblique Tenotomy and Inferior Oblique Recession in Brown's Syndrome

The technique and results of simultaneous superior oblique tenotomy and 14-mm inferior oblique recession for true Brown's syndrome are presented for 16 eyes of 13 patients. A good or excellent result was achieved in 15 of 16 eyes (94%). Reoperation for overcorrection was not necessary; however, repeat tenotomy was required in two cases. Inferior oblique underaction was present in 12 of 16 eyes (75%) in the early postoperative period; however, elevation in adduction improved over time. At most recent examination, 92% of eyes demonstrated greater than 25° elevation in adduction. Underaction of the superior oblique occurred in 3 of 16 eyes (19%). A simultaneous superior oblique tenotomy and inferior oblique recession is recommended in all patients selected to undergo surgery for true Brown's syndrome to prevent reoperation for iatrogenic superior oblique palsy.

Repairing the Superior Oblique Tendon-Reply

In Reply. —Dr Kopf's question highlights some difficulties involved in managing superior oblique paresis combined with restriction of upgaze in adduction. In managing both our cases, we did not wish to exacerbate the patients' poor elevation in adduction and, therefore, we did not weaken the ipsilateral inferior oblique muscle. In the first case, weakening of the ipsilateral superior rectus muscle at the initial procedure successfully diminished the vertical deviation and left the contralateral inferior rectus muscle available for a subsequent procedure. We learned from the first case that the initial procedure to free the restriction of the damaged superior oblique tendon is followed by months of gradual reduction of the restriction (aided by a functioning inferior oblique muscle) and gradual progression of the superior oblique paresis. Because of this, when faced with the second case, we did not attempt to address the vertical deviation at all during the initial procedure

SUPERIOR OBLIQUE TUCK FOR SUPERIOR OBLIQUE PALSY

Fifty-nine patients with a superior oblique palsy had a superior oblique tuck as part of their surgical treatment. The average size of the tuck was 12.0 mm. All cases had a decrease in the hyperdeviation in the primary position and some decrease in elevation in adduction in the operated eye (Brown's syndrome). Seventeen per cent of the patients required take-down of the tuck three to 24 months after surgery (average time for reoperation, 9.1 months). Symptoms forming indications for take down of the tuck were head tilt, vertical diplopia, torsional diplopia, and a tight feeling on elevation in adduction. No patient who had a tuck alone required take-down. Brown's syndrome was more likely to occur in cases with weakening of the antagonist inferior oblique and when a bilateral tuck of the superior oblique had been done. Taking down of the tucked tendon relieved the symptoms of Brown's syndrome in seven of 10 patients, without a recurrence of superior oblique underaction. After superior oblique tuck in all patients, a residual vertical deviation could be measured and in nearly every case a Brown's syndrome could be found.

Traumatic Simulated Brown's Syndrome: A Case Report

A case report of a simulated Brown's tendon sheath syndrome is presented which masks as an orbital floor fracture with entrapment. Despite a positive forced traction test, additional diagnostic information such as a normal tomographic exam of the orbital floor, vertical saccadic up gaze velocity measurements consistent with edema and hemorrhage, greater limitation to elevation in adduction than abduction, and tenderness and soft tissue injury in the region of the trochlea, persuaded us to conservatively manage this case. It behooves the ophthalmologist to consider a temporary superior restrictive phenomenon produced by edema prior to any surgical approach to improve elevation of the globe.

Superior Oblique Tendon Sheath Syndrome of Brown

Twenty-four patients with true superior oblique tendon sheath syndrome (Brown's syndrome) were extensively examined surgically. Since a tight or short anterior sheath of the superior oblique tendon was not present in any of our cases, we are not able to support the theory that this form of the syndrome is due to a congenital anomaly of the anterior sheath. The superior oblique tendon was taut and shortened in only two cases; in all the others it was limp, even in attempts to elevate the eye passively in adduction. Thus the majority of cases of constant congenital Brown's syndrome remain unexplained with no obvious abnormality found at surgery in any of the six extraocular muscles. However, our surgical findings did suggest that a restrictive band posterior and inferior to the globe was responsible for the limited elevation in adduction.

Surgical treatment of the superior oblique tendon sheath syndrome.

Temporary passive traction sutures holding the eye into elevation enhanced the success of operations to remove the short superior oblique tendon sheath which was restraining elevation in adduction (Brown's syndrome). The technique, results, and complications of surgery are discussed.

Duane's syndrome. An electromyographic study.

Medial rectus innervation was always normal, and lateral rectus innervation was always abnormal. Lateral rectus overactivity accompanied deficient adduction. Lateral rectus underactivity accompanied abduction deficiency and was reflected in slowed saccadic abduction movements. Secondary contractures of the medial rectus and lateral rectus were often present. Lateral rectus overactivity with upgaze, downgaze, or both, caused A, V, or X patterns. Retraction on adduction was accompanied by abnormal activity of the superior rectus, inferior rectus, or lateral rectus. Elevation in adduction was usually caused by abnormal superior rectus activity and not abnormal inferior oblique activity. Narrowing of the palpebral fissure only occurred with retraction of the eye. Levator and orbicularis innervations did not change with adduction.