Many vertical deviations are characterized by a hypertropia that is much greater on gaze to one side. They are often, but not exclusively, associated with oblique muscle abnormalities.
Overelevation and Overdepression in Adduction
There are several causes of overelevation in adduction (OEAd) and overdepression in adduction (ODAd) (Tables 11-1, 11-2). These include true overaction and underaction of the oblique muscles, as well as several conditions that can simulate oblique muscle overactions. These cases have also been termed oblique muscle pseudo-overactions.
In some patients, such as those with large-angle exotropia or thyroid eye disease, clinical examination of versions appears to show overaction of both the superior and the inferior oblique muscles. In such cases, elevation or depression of the vertical rectus muscle of the opposite, abducting eye is restricted in the lateral portion of the bony orbit. The clinical findings can be explained as an attempt by the vertical rectus muscle to overcome this restriction through extra innervation, which, according to Hering’s law, is distributed to the yoke oblique muscle as well (see Chapter 4). Alternatively, overelevation may be due to slippage of a tight lateral rectus muscle as the eye adducts and rises above or below the midline (see Chapter 10).
Table 11-1 Causes of Overelevation in Adduction
Table 11-2 Causes of Overdepression in Adduction
Malposition of the rectus muscle pulleys can lead to anomalous movements that can simulate oblique muscle overactions. This can be seen in craniofacial syndromes. For example, an inferiorly displaced lateral rectus muscle pulley can cause depression in abduction or, if this is the fixating eye, OEAd of the contralateral eye and a V-pattern deviation that simulate inferior oblique muscle overaction. Conversely, a superiorly displaced lateral rectus muscle can produce ODAd—simulating a superior oblique overaction—along with an A-pattern deviation. Lateral and medial malpositioning of vertical rectus muscles can also create pseudo-overactions of oblique muscles. The treatment implication is that apparent oblique dysfunction or A and V patterns associated with anomalous pulley positions respond poorly to oblique muscle surgery.
Other causes of OEAd and ODAd include the upshoots and downshoots of Duane retraction syndrome, superior or inferior rectus muscle restriction (causing extra innervation of contralateral oblique muscles), limitation of elevation in abduction after inferior oblique anterior transposition (anti-elevation syndrome), and rare cases of Brown syndrome.
Inferior oblique muscle overaction
Overaction of the inferior oblique muscle is one cause of OEAd. The overaction is termed primary when it is not associated with superior oblique muscle palsy. It is called secondary when it accompanies palsy of the superior oblique muscle or the contralateral superior rectus muscle. The eye is elevated in adduction, both on horizontal movement and in upgaze (Fig 11-1).
One explanation of primary overaction relates to vestibular factors governing postural tonus of the extraocular muscles. Some authors have questioned whether primary inferior oblique overaction truly exists, preferring to describe the movement merely as OEAd.
Clinical features Primary inferior oblique muscle overaction has been reported to develop between ages 1 and 6 years in up to two-thirds of patients with infantile strabismus (esotropia or exotropia). It also occurs, less frequently, in association with acquired esotropia or exotropia and, occasionally, in patients with no other strabismus. Bilateral overaction can be asymmetric, often in patients with poor vision in 1 eye, which leads to greater overaction in that eye.
With the eyes in lateral gaze, alternate cover testing shows that the higher (adducting) eye refixates with a downward movement and that the lower (abducting) eye refixates with an upward movement. When inferior oblique muscle overaction is bilateral, the higher and lower eyes reverse their direction of movement in the opposite lateral gaze. These features differentiate inferior oblique overaction from DVD, in which neither eye refixates with an upward movement, whether adducted, abducted, or in primary position. A V-pattern horizontal deviation (see Chapter 10) and extorsion are common with overacting inferior oblique muscles.
Figure 11-1 Bilateral inferior oblique muscle overaction. Overelevation in adduction, seen best in the upper fields of gaze.
(Courtesy of Edward L. Raab, MD.)
Management For cases in which inferior oblique overaction produces a functional problem—V-pattern strabismus, hypertropia in primary position, or symptomatic hypertropia in side gaze—a procedure to weaken the inferior oblique muscle (recession, disinsertion, myectomy, or anterior transposition) is indicated. Some surgeons grade the weakening procedure according to the severity of the overaction. Weakening of the inferior oblique muscles generally has an insignificant effect on horizontal alignment in primary position.
Superior oblique muscle overaction
Superior oblique muscle overaction is one of several causes of ODAd.
A vertical deviation in primary position often occurs with unilateral or asymmetric bilateral overaction of the superior oblique muscles. The lower eye has the overacting superior oblique muscle in unilateral overaction and the more prominently overacting superior oblique in bilateral cases. The overacting superior oblique muscle causes a hypotropia of the adducting eye, which is accentuated in the lower field of gaze (Fig 11-2). A horizontal deviation, most often exotropia, may be present and may lead to an A pattern (see Chapter 10). Intorsion is common with superior oblique muscle overaction. Most cases of bilateral superior oblique overaction are primary overactions.
In a patient with clinically significant hypertropia or hypotropia or an A pattern, a procedure to weaken the superior oblique tendon (recession, tenotomy, tenectomy, or lengthening by insertion of a silicone spacer or nonabsorbable suture or by split-tendon lengthening) is appropriate. Significant intorsion will also be reduced with any of these procedures. Many surgeons are reluctant to perform superior oblique tendon weakening in patients with fusion because torsional or asymmetric vertical effects can cause diplopia. As with inferior oblique muscle overaction, the horizontal deviation can be corrected during the same operative session. Some surgeons, anticipating a convergent effect in primary position, alter the amount of horizontal rectus muscle surgery when simultaneously weakening the superior oblique muscles.
Top row, Bilateral superior oblique muscle overaction. Overdepression in adduction, seen best in the lower fields of gaze. Bottom row, Associated bilateral inferior oblique underaction.
(Courtesy of Edward L. Raab, MD.)
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.