Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006

tional pull on the dependent side of the face causes changes in size of facial structures. Another theory is that facial asymmetry represents a mild form of congenital plagiocephaly associated with the superior oblique palsy.

In summary, signs that a superior oblique palsy is congenital and not acquired include childhood photographs showing a long-standing head tilt, facial asymmetry, lack of extorsional diplopia, lack of extorsion by Maddox rod, and large vertical fusion amplitudes. In most cases, the diagnosis of congenital superior oblique muscle palsy can be made on the basis of clinical evaluation.

Other Causes of Superior Oblique Paresis

The majority of superior oblique pareses are either congenital or traumatic, but other causes include vascular disease with brainstem lacunar infarcts, multiple sclerosis, intracranial neoplasm, herpes zoster ophthalmicus, diabetes and associated mononeuropathy, and iatrogenic after superior oblique tenotomy. An acquired idiopathic superior oblique paresis requires a neurological workup including neuroimaging. Patients with craniosynostosis may have bilateral superior oblique palsies caused by absent superior oblique tendons.

Treatment of Superior Oblique Paresis

The treatment of superior oblique paresis depends on the pattern of the strabismus. Cardinal position of gaze measurements and evaluation for inferior oblique overaction and superior oblique underaction are needed to determine the pattern of strabismus and where the deviation is greatest. Subjective torsion should be assessed by double Maddox rod testing in acquired cases; however, patients with a congenital superior oblique palsy will not have subjective torsion. Objective torsion evaluated by indirect ophthalmoscopy can be useful for verifying torsional abnormalities but is usually not the major clinical sign that directs the treatment plan.

Most treatment strategies require identifying where the hypertropia is greatest, and surgery is then designed to correct the deviation in primary position while reducing the incomitance.15 For example, a right unilateral superior oblique paresis with a hypertropia less than 10 PD in primary position, inferior oblique overaction, and minimal superior oblique underaction

be used when tucking the superior oblique, as iatrogenic Brown’s syndrome is a frequent complication of a superior oblique tendon tuck. Most surgeons avoid the superior oblique tuck unless there is significant superior oblique underaction and an extremely lax tendon or, in cases of bilateral superior oblique paresis, where there is severe superior oblique underaction.

Traumatic superior oblique palsies should be observed for 6 months following recovery of muscle function. Patients who have partial recovery of superior oblique muscle function will often be left with extorsional diplopia worse in downgaze, without significant oblique dysfunction, V-pattern, or hypertropia. In these cases, extorsion can be improved by the Harada–Ito procedure, which consists of selectively tightening the anterior one-fourth to one-third of the superior oblique tendon fibers.11 Patients with a bilateral superior oblique palsy and poor recovery of muscle function show a large esotropia in downgaze (arrow subtype V-pattern), extorsion greater in downgaze, left hypertropia in rightgaze, and a right hypertropia in leftgaze, but minimal or no hypertropia in primary position. In these cases, consider either bilateral Harada–Ito procedures and bilateral medial rectus muscle recessions with infraplacement one-half-tendon-width or bilateral superior oblique tendon tucks and bilateral medial rectus muscle recessions with infraplacement one-half-tendon-width. This is a difficult strabismus to correct; however, surgery can often improve diplopic symptoms. The superior oblique tucks will create a bilateral iatrogenic Brown’s syndrome, but this may be an acceptable trade-off for improved single binocular vision in downgaze. Table 9-4 lists treatment strategies for unilateral superior oblique paresis, and Table 9-5 lists treatments for bilateral superior oblique paresis.

Inferior Oblique Paresis

An isolated inferior oblique paresis is extremely rare and, when it does occur, it is usually idiopathic. Pollard28 reported on 25 patients having an isolated inferior oblique palsy, with 23 being unilateral and 2 bilateral. All cases were idiopathic and benign without an identifiable neurological cause. Rarely, inferior oblique palsy has been reported after head trauma20 or attributed to a microvascular occlusive event. Patients with isolated inferior oblique paresis show ipsilateral superior oblique overaction, but they can be distinguished from those with primary superior

superior oblique tendon expander) if the hypotropia is less than 10 PD, or add a recession of the contralateral superior rectus recession if the hypotropia is greater than 10 PD.30

Superior Oblique Overaction

The cause of superior oblique overaction (SOOA) is unknown. It may be related to an associated paresis of the contralateral inferior rectus muscle, thus producing a secondary overaction of the yoke superior oblique muscle. The author has noted several patients with superior oblique overaction who also have an underacting contralateral inferior rectus muscle.

CLINICAL FEATURES OF SUPERIOR OBLIQUE OVERACTION

Superior oblique overaction is an exaggeration of the normal function of the superior oblique muscle that includes intorsion, depression, and abduction. Patients with superior oblique overaction show a downshoot of the adducting eye in lateral gaze, abduction in downgaze causing an A-pattern, and intorsion that is seen on indirect ophthalmoscopy. The A-pattern is not symmetrical, but shows more divergence from primary position to downgaze than from upgaze to primary position. This type of A- pattern is termed a lambda pattern (Fig. 9-8).

TREATMENT OF SUPERIOR OBLIQUE OVERACTION

The ideal superior oblique weakening procedure produces a measured slackening of the muscle–tendon complex without disrupting the functional mechanics of the insertion. Many surgical approaches to weaken the superior oblique have been tried.3,31 Presently, the two procedures most commonly used are the superior oblique tenotomy and the Wright silicone tendon expander.38,41 The tenotomy technique involves cutting the tendon in two, while the silicone tendon expander consists of inserting a segment of a 240 retinal silicone band (4–6 mm) between the cut ends of a nasal tenotomy to elongate the tendon.42

Other superior oblique weakening procedures include tenectomy, recession, and posterior tenotomy.3,31 In a comparative study, this author found the silicone tendon expander procedure to be superior to a tenotomy, especially in patients with preoperative fusion.40 Performing a superior oblique tenotomy on patients with high-grade stereopsis and fusion carries a significant risk for creating a secondary superior oblique paresis and causing postoperative diplopia.25 In these cases, the silicone tendon expander is preferred. Another situation where superior oblique weakening procedures can cause problems is in patients with preexisting dissociated vertical deviation (DVD); weakening the superior obliques will exacerbate DVD. In these cases, options are to treat the A-pattern with horizontal rectus muscle transpositions rather than weakening the superior obliques, or to plan an undercorrection of the superior oblique overaction with the silicone tendon expander. The advantage of the superior oblique silicone tendon expander is that it lengthens the superior oblique tendon in a controlled manner and holds the cut tendon ends apart at a fixed distance. This technique reduces postoperative superior oblique paresis, allows for controlled weakening, and makes it possible to find cut tendon ends if a reoperation is necessary.

Inferior Oblique Overaction

Primary inferior oblique overaction is most commonly associated with a horizontal strabismus such as congenital esotropia or intermittent exotropia. Isolated primary inferior oblique overaction can also occur without associated horizontal strabismus.

Although primary inferior oblique overaction is bilateral, in

occurs because the inferior oblique muscles act as abductors in upgaze. In contradistinction, a V-pattern associated with superior oblique paresis (especially bilateral) shows an arrow pattern with an esotropic shift that occurs when moving from primary position to downgaze. Because the inferior oblique muscle is an extortor, elevator, and abductor, these elements are exaggerated in direct proportion to the overaction. When quantitating inferior oblique overaction, look at the entire function of the muscle, including the upshoot, amount of V-pattern, and fundus extorsion.10,37

See Table 9-3 for a comparison of the clinical signs of primary inferior oblique overaction with secondary inferior oblique overaction caused by superior oblique paresis.

MIMICKERS OF INFERIOR OBLIQUE OVERACTION

Inferior oblique overaction is the most common cause of an ocular upshoot in adduction. Dissociated vertical deviation (DVD) can look just like inferior oblique overaction, because DVD will become manifest in sidegaze as the adducted eye is occluded by the nasal bridge (see Chapter 10); this results in a hyperdeviation in sidegaze that mimics inferior oblique overaction. DVD can be differentiated from inferior oblique overaction by occluding the affected eye in abduction as well as adduction and evaluating for a change in the vertical deviation. If the elevation is the same in adduction and abduction, then this is DVD, whereas an increasing hyperdeviation in adduction suggests inferior oblique overaction. Because DVD commonly coexists with inferior oblique overaction in patients with infantile esotropia, the distinction can be extremely difficult to see. Distinguishing clinical features such as the presence of a V- pattern (Y-subtype), a true hyperdeviation in lateral gaze with a hypotropia of the contralateral eye, and objective extorsion on indirect ophthalmoscopy will help to identify inferior oblique overaction rather than DVD.

An upshoot in adduction can be caused by a tight lateral rectus muscle. As the eye adducts and slightly elevates, the tight lateral rectus pulls the eye up, causing pseudo-overaction of the inferior oblique. Aberrant innervation of the inferior oblique and superior rectus muscles has been documented as causing an upshoot associated with Duane’s syndrome (see Chapter 10).