Unilateral superior oblique palsy

In a unilateral palsy, the hyperdeviation is typically incomitant, especially in the acute stages. Over time, contracture of the ipsilateral superior rectus or contralateral inferior rectus muscle can lead to “spread of comitance,” with the result that there is minimal difference in the magnitude of the hypertropia when the patient looks from one side to the other. If depression cannot be evaluated because of the eye’s inability to adduct (eg, in third nerve palsy), superior oblique muscle function can be evaluated by observing whether the eye intorts, as judged by the movement of surface landmarks or examination of the fundus, when the patient attempts to look downward and inward from primary position. Weakness of the superior oblique muscle also results in extorsion of the eye. If the degree of extorsion is large enough, subjective incyclodiplopia, in which the patient describes the image as appearing to tilt inward, can occur.

The diagnosis of unilateral superior oblique muscle palsy is further established by results of the 3-step test (also called the Parks-Bielschowsky 3-step test) (Fig 11-3; see also Chapter 7, Fig 7-8) and the double Maddox rod test to measure torsion. However, results of the 3-step test can be confounded in patients with DVD, entities involving restriction, additional paretic muscles, previous strabismus surgery, or skew deviation. Intorsion of the higher eye on fundus examination—instead of the expected extorsion—suggests skew deviation, especially when there are associated neurologic findings. In addition, if the patient is placed in a supine position, the vertical tropia is more likely to decrease with skew deviation than with superior oblique palsy. Some ophthalmologists document serial changes in the deviation by means of the Hess screen or the Lancaster red-green test or by plotting the field of single binocular vision. (See Chapter 7 for further discussion of some of the tests mentioned in this section.)

Inhibitional palsy of the contralateral antagonist

Patients who fixate with the paretic eye can exhibit so-called inhibitional palsy of the contralateral antagonist (Fig 11-4). If a patient with right superior oblique palsy uses the right eye to fixate on an object that is located up and to the left, the innervation of the right inferior oblique muscle required to move the eye into this gaze position is reduced because the right inferior oblique muscle does not have to overcome the normal antagonistic effect of the right superior oblique muscle (Sherrington’s law). According to Hering’s law, less innervation is also received by the yoke muscle of the right inferior oblique muscle, which is the left superior rectus muscle. This decreased innervation can lead to the impression that the left superior rectus muscle is paretic.

Figure 11-3 Right superior oblique palsy. There is a right hypertropia in primary position that increases in left gaze and with head tilt to the right. Note accompanying overaction of the right inferior oblique muscle.

(Courtesy of Edward L. Raab, MD.)

Figure 11-4 Palsy of right superior oblique muscle. A, With the palsied right eye fixating, little or no vertical difference appears between the 2 eyes in the right field of gaze (1 and 4). In primary position (3), a left hypotropia may be present because the right elevators require less innervation to stabilize the eye in primary position, and thus the left elevators will receive less-than-normal innervation. When gaze is up and left (2), the RIO needs less-than-normal innervation to elevate the right eye because its antagonist, the RSO, is palsied. Consequently, its yoke, the LSR, will be apparently underacting, and pseudoptosis with pseudopalsy of the LSR will be present. When gaze is toward the field of action of the palsied RSO muscle (5), maximum innervation is required to move the right eye down during adduction, and thus the yoke LIR will be overacting. B, With the unaffected left eye fixating, no vertical difference appears in the right field of gaze (1 and 4). In primary position (3), the right eye is elevated because of unopposed elevators. When gaze is up and left (2), the RIO shows marked overaction because its antagonist is palsied. The action of the LSR is normal. When gaze is down and left (5), normal innervation required by the fixating normal eye does not suffice to fully move the palsied eye into that field of gaze. (See also Chapter 7, Fig 7-8.) LIO = left inferior oblique; LIR = left inferior rectus; LSO = left superior oblique; LSR = left superior rectus; RIO = right inferior oblique; RIR = right inferior rectus; RSO = right superior oblique; RSR = right superior rectus.

(Reproduced with permission from von Noorden GK. Atlas of Strabismus. 4th ed. St Louis: Mosby; 1983:24–25.)

Bilateral superior oblique palsy

Bilateral superior oblique palsy occurs commonly after head trauma but is sometimes congenital. It can be differentiated from unilateral superior oblique muscle palsy by the following criteria:

• Unilateral cases usually show little if any V pattern and less than 10° of extorsion in downgaze. Subjective incyclodiplopia is uncommon. The Bielschowsky head-tilt test (step 3 of the 3-step test) yields positive results for the involved side only. Abnormal head positions—usually a tilt toward the shoulder opposite the side of the weakness—are common. The oblique muscle dysfunction is confined to the involved eye.

• Bilateral cases usually show a V pattern. Extorsion is 10° or more in downgaze; more than 15° of extorsion in primary position is highly suggestive of bilateral involvement. Subjective incyclodiplopia is common in acquired bilateral cases. The Bielschowsky head-tilt test yields positive results on tilt to each side—that is, right head tilt produces a right hypertropia and left head tilt, a left hypertropia. There is bilateral oblique muscle dysfunction. Patients may exhibit a chin-down head position. Symmetric palsies may show little or no hypertropia in primary position.

Unilateral superior oblique muscle palsy

There are many options for surgical treatment of a unilateral palsy. Any of the 4 cyclovertical muscles in each eye could potentially be operated on to correct the hypertropia. Some surgeons use a uniform approach and weaken the ipsilateral antagonist inferior oblique muscle. For other surgeons, the surgical plan is informed by superior oblique tendon laxity. Tendon laxity is assessed at the time of surgery by forced duction testing, in which the globe is pushed (translated) posteriorly into the orbit while it is simultaneously extorted, thus placing the superior oblique tendon on stretch (Video 11-1). If the tendon is lax, they perform a superior oblique tightening procedure; if it is not, they usually perform an inferior oblique weakening procedure. Other ophthalmologists use tendon laxity only as diagnostic confirmation of superior oblique palsy.

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Many surgeons take a tailored approach, reflecting the variety of hypertropia patterns that may occur with superior oblique palsy. For example, if underaction of an affected right superior oblique muscle is the most prominent feature, then the deviation will be greatest in down-left gaze. Another patient, by contrast, may predominantly exhibit overaction of the antagonist inferior oblique muscle, with the greatest deviation in up-left gaze. Because each of the 8 cyclovertical muscles has a somewhat different field of action, surgery involving some muscles will be more appropriate than others, depending on the field of gaze in which the deviation is largest (Table 11-3). In addition, some surgeons believe that superior oblique tightening is the most effective procedure for addressing a marked head tilt in children with congenital superior oblique palsy. Extorsion in unilateral superior oblique palsy rarely produces symptoms, but when it does, it can be corrected with a Harada-Ito procedure.

If the hyperdeviation is greater than 15 prism diopters (Δ) in primary position, surgery usually involves at least 2 muscles. Ipsilateral inferior oblique weakening and superior oblique tightening represent a particularly powerful combination but carry an increased risk of problematic iatrogenic Brown syndrome or overcorrection. In the unusually severe case with a vertical deviation greater than 35Δ in primary position, 3-muscle surgery is usually required.

Whatever the approach, it is important to avoid overcorrection of a long-standing unilateral superior oblique muscle palsy. Because there are often no sensory or motor adaptations to hypertropia in the opposite direction, disabling diplopia can result.

Bilateral superior oblique muscle palsy

Surgical planning for treatment of bilateral superior oblique muscle palsy can be complex. If the paresis is asymmetric, hypertropia in primary position may be present and require many of the same considerations as hypertropia in unilateral palsy. In addition, there is often symptomatic extorsion or a V pattern that needs to be addressed.

If the palsies are symmetric (minimal hypertropia in primary position), both inferior oblique muscles can be weakened if they are overacting and hypertropia is present in side gaze. Bilateral superior oblique muscle tightening should be performed when hypertropia in side gaze is accompanied by V-pattern esotropia or symptomatic extorsion, especially in downgaze. If there is symptomatic extorsion but minimal hypertropia in side gaze, bilateral Harada-Ito procedures can be performed. Other, less commonly used approaches, such as bilateral inferior rectus muscle recessions, serve to add extra innervational drive on downgaze to help overcome the superior oblique deficits.

Table 11-3 Surgical Treatment of Unilateral Superior Oblique Palsy

Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.