Superior Oblique Tendon Sheath Syndrome Research Articles

Brown Syndrome or Superior Oblique Tendon Sheath Syndrome: Radiologic Imaging Characteristics and Literature Review

Brown syndrome is the inability to gaze upward beyond the horizontal level while adducting the eye due to an abnormality of the superior oblique tendon sheath complex. It is a rare extraocular muscular disorder, and its imaging is infrequently seen in radiologic practice. This article presents clinical characteristics and imaging of 5 patients with Brown syndrome and reviews the radiologic literature available, to familiarize the readers with its imaging findings.

Orbital MRI in Superior oblique tendon sheath syndrome (Brown's syndrome)

Durch Kontraktion des Musculus obliquus superior wird der Blick nach unten und außen gerichtet, und zwar durch Abduktion, Herabsenken und Innenrotation des Auges.

Brown’s Syndrome in the absence of an intact superior oblique muscle

Brown’s Syndrome was initially described as a superior oblique tendon sheath syndrome—a short anterior tendon resulting in a restricted elevation of the globe in the nasal field. Brown believed that a congenital paralysis of the inferior oblique muscle resulted in this secondary shortening of the anterior sheath of the superior oblique tendon. 1 The definition of Brown’s Syndrome has changed over time. It is currently defined as the inability to elevate the eye in the adducted position, both actively and passively on force duction testing, and can be acquired. 2 The pathophysiology of acquired Brown’s Syndrome may involve an abnormality of the superior oblique trochlea/tendon complex. However, it may also result from other causes unrelated to the superior oblique tendon or muscle, such as tumors of the superior nasal orbit, inferior orbital mechanical restriction, or an inferiorly displaced lateral rectus muscle and pulley. 3,4 We present two cases in which a Brown’s Syndrome was diagnosed after the superior oblique muscle had been disinserted or removed.

Superior oblique tendon expansion in the management of superior oblique dysfunction.

Traditional superior oblique weakening procedures may be unpredictable and lead to superior oblique underaction. The use of 240 retinal band as a spacer to lengthen the superior oblique tendon has been proposed as a more controlled approach than superior oblique tenotomy and related procedures. The use of this technique is reported in a patient with diplopia following an orbital floor blow out fracture, and in a child with Brown's superior oblique tendon sheath syndrome.

Surgical Results in Brown Syndrome

Surgical treatment for Brown superior oblique tendon sheath syndrome, now called Brown syndrome, has been advocated for patients with abnormal head posture or manifest hypotropia in primary gaze. Several surgical procedures with variable results and complications have been reported without consensus. Techniques and results of treatment for Brown syndrome at two institutions were reviewed. Charts of all patients who had undergone surgical treatment at Texas Children's Hospital, Houston, Tex, and Riley Hospital for Children, Indianapolis, Ind, between 1965 and 1989 were reviewed. The review yielded 38 patients. Superior oblique tenectomy was the most efficacious initial procedure. Surgery was successful in the treatment of anomalous head posture associated with Brown syndrome. There was no loss of sensory function as a result of surgery, but surgery did not inevitably lead to improved sensory function. We do not advocate superior oblique weakening combined with simultaneous surgery for iatrogenic superior oblique palsy as an initial procedure for Brown syndrome, since nearly one-half of our patients did not develop superior oblique palsy when followed for more than 1 year.

Computed tomography in the evaluation of Brown syndrome of the superior oblique tendon sheath.

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.

Superior Oblique Tenectomy in Brown's Syndrome

Since its description in 1950, numerous surgical techniques have been advocated to treat Brown's superior oblique tendon sheath syndrome. Of these, a tenectomy of the homolateral superior oblique has emerged as the most effective method. However, an iatrogenically produced superior oblique paralysis has been found to be a frequent complication of this procedure. Of 12 patients with Brown's syndrome treated with a superior oblique tenectomy, this problem was encountered in eight patients, and additional surgery became necessary in each instance. The clinical management of such patients presents special problems and their solution will be illustrated by two case reports.

Surgical Treatment of True Brown's Syndrome

In 1950 H. W. Brown reported the superior oblique tendon sheath syndrome and cut the sheath as treatment for the condition. My results (as well as those of other surgeons) with similar surgery have been disappointing. Consequently, I carried out different operations consisting of Z tenotomy of superior oblique tendon in nine patients, split tendon lengthening in two patients, complete tenotomy in 16 patients, and a tenectomy in two patients. One of the latter was done on a patient after an unsatisfactory tenotomy where I missed the tendon. Tenotomy of the superior oblique tendon gave the best results. Experiments with the superior oblique tendon in cadavers several hours after death showed that after cutting the tendon just medial to the superior rectus muscle, the cut end of the tendon moved medially only about 8 to 10 mm due to restrictions of the capsular attachments to the trochlea. The cause of "true" Brown's syndrome is a tight tendon, and a safe and effective surgical treatment consists of cutting it just medial to the superior rectus muscle.

Superior oblique tendon sheath syndrome.

Clinical examination of 15 patients with the superior oblique tendon sheath syndrome showed that 12 of them had some evidence of stenosing tenosynovitis.

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.

Acquired intermittent Brown's syndrome.

A 29-year-old woman and an 11-year-old boy had episodic vertical diplopia of recent onset. In both a neurologic condition was suspected initially; however, intermittent Brown9s superior oblique tendon sheath syndrome was diagnosed. Both patients reported improvement after eye exercises. The importance of recognizing this entity in the differential diagnosis of acquired diplopia is evident.

True and simulated superior oblique tendon sheath syndromes.

Summary The superior oblique tendon sheath syndrome can be divided into two groups—true and simulated. The true cases have positive forced-duction tests and are caused by a congenitally short anterior sheath of the superior oblique tendon. Simulated cases are caused by a congenital structural anomaly of the posterior tendon or by an abnormal firm attachment of the sheath to the posterior tendon, or to both. Acquired and intermittent sheath syndromes are of inflammatory origin and subject to spontaneous recovery. An operation is not indicated in the absence of a disfiguring head tilt or a vertical atropia, but the operative techniques are described for appropriate cases.

Superior oblique tendon sheath syndrome and its relationship to stenosing tenosynovitis.

Superior oblique tendon sheath syndrome and its relationship to stenosing tenosynovitis.

Simulated Superior Oblique Tendon Sheath Syndrome Following Orbital Floor Fracture

Simulated Superior Oblique Tendon Sheath Syndrome Following Orbital Floor Fracture

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.

Unusual sequelae of surgery in the superior oblique tendon sheath syndrome.

Unusual sequelae of surgery in the superior oblique tendon sheath syndrome.

Bilateral superior oblique tendon sheath syndrome. Occurrence and spontaneous recovery in one of uniovular twins.

Bilateral superior oblique tendon sheath syndrome. Occurrence and spontaneous recovery in one of uniovular twins.

THE INTRAOPERATIVE FORCED DUCTION TEST. REPORT OF A CASE OF CONGENITAL FIBROUS BANDS.

Mechanical anomalies as a cause of strabismus are well known. These include entities involving the muscles such as Duane's syndrome and strabismus fixus as well as abnormalities of the fascial attachments such as Brown's superior oblique tendon sheath syndrome, Johnson's adherence syndrome, and the varied anomalies of check ligaments described so fully by Scobee. The value of a preoperative forced duction test in these as well as any case in which there is limitation of rotation is obvious. The purpose of this report is to present a case of congenital restricting fibrous bands and to draw attention to the importance of the intraoperative as well as preoperative forced duction test in the evaluation of cases of limited motility. Report of Cases Case 1.—History. —A 13-year-old female was first seen at age 9. Having been raised by a guardian, there is no history of pregnancy or birth difficulties. Ptosis and muscle

Superior oblique tendon sheath syndrome.

At the strabismus symposium in Iowa City in 1950, Brown presented a preliminary report on a new syndrome, 1 which he referred to as the superior oblique tendon sheath syndrome. At the more recent symposium, in New Orleans, he amplified his original presentation and stated that the following criteria were necessary for the diagnosis: paralysis of the inferior oblique, little or no overaction of the superior oblique, depression of the eye on adduction, and limitation to passive elevation of the adducted eye. Brown believed that the syndrome was due to a congenitally short sheath of the superior oblique. Whitnall 2 has shown that the sheath is firmly attached to the trochlea. With the eye straight or abducted, the sheath is loose and allows full rotations. However, when the eye is adducted the congenitally short sheath acts as a tight band which prevents elevation.