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

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Ocular Restriction

Classically, the term ocular restriction describes a mechanical tether or leash that limits ocular rotations. Ocular restriction, however, can be caused by at least two general mechanisms: a mechanical tether on eye movements or misdirected muscle forces that work against the normal agonist muscle function. The term restriction is often loosely used as a general term for limited eye movements; however, a clear distinction should be made between ocular restriction and rectus muscle palsy. If the cause of diminished eye movements is not known, then use the term limited rotations or limitation of eye movements until the etiology is determined. Table 10-2 lists the causes of restrictive strabismus.

Mechanical restriction of eye movement is caused by adhesions to an extraocular muscle or sclera, a tight or inelastic extraocular muscle, or an orbital mass. Restrictive adhesions can occur from conjuctival scarring, scarring of Tenon’s capsule, orbital fat adherence, and, rarely, congenital fibrotic bands that attach to the eye or extraocular muscles. Inelastic muscle or muscle fibrosis occurs with thyroid myopathy, local anesthesia myotoxicity, and congenital muscle fibrosis (e.g., monocular elevation deficit and congenital fibrosis syndrome). An orbital mass, such as an orbital hemangioma, or a glaucoma implant can cause ocular restriction either by direct interference of rotation of the eye or by pressure on an extraocular muscle that tightens the muscle. Restriction resulting from misdirected muscle force vectors occurs in conjunction with aberrant innervation of an antagonist muscle and abnormal muscle–pulley location or a displaced extraocular muscle.20,25,83 An example of aberrant innervation causing restriction is limited adduction, often associated with Duane’s syndrome. Restricted adduction occurs because the lateral rectus muscle is aberrantly innervated by part of the medial rectus nerve. When the eye attempts to adduct, the lateral rectus muscles contracts against the contracting medial rectus muscle, thus restricting adduction.

An example of displaced extraocular muscle is the V-pattern strabismus and superior oblique muscle underaction that are frequently seen in patients with craniosynostosis.20 These patients have excyclorotation of the orbits that results in superior displacement of the medial rectus muscle and limited ocular depression in adduction. The superiorly displaced medial rectus muscle pulls the eye up in addition to its normal function of

adduction and limits depression in the field of action of the superior oblique.20 A rare example of restriction caused by a displaced muscle–pulley was reported by Oh et al.83 They described a patient with limitation of elevation in adduction, or a pseudoBrown’s syndrome, caused by a congenitally inferiorly displaced lateral rectus muscle and its pulley. These authors hypothesized that the infraplaced lateral rectus muscle and pulley act to pull the eye down, limiting elevation on adduction. Iatrogenic displacement of extraocular muscles during strabismus surgery can also cause limited eye movements. Inferior oblique muscle anteriorization anterior to the inferior rectus insertion can also cause active restriction and limited elevation (see Chapter 2, Fig. 2–17).15,43,114,135 In some cases, restriction and paresis coexist, such as with paretic lateral rectus muscle and secondary contracture of its antagonist medial rectus muscle. It is important to diagnoses the cause of limited ductions to formulate an effective surgical plan. The next section describes methods for diagnosing extraocular muscle paresis and ocular restriction.

Diagnosing Restriction Versus Paresis

The principal diagnostic tests that differentiate paresis from restriction include saccadic velocity measurements, forced ductions, and forced-generation test. Other signs influencing diagnosis include intraocular pressure changes in various fields of gaze and lid fissure changes in sidegaze.

SACCADIC VELOCITY MEASUREMENTS

Saccadic velocity measurements can help differentiate restriction from paresis by observation, without touching the eye. Therefore, this method is useful in young children as well as adults. Saccadic movements are fast, jerk-like eye movements that require normal rectus muscle function. The rectus muscles are the major movers of the eye and are responsible for saccadic eye movements. The presence of a saccadic eye movement indicates normal rectus muscle function whereas the inability to stimulate a saccade suggests a rectus muscle palsy. A paretic rectus muscle does not have the power to generate a saccadic eye movement, and the eye drifts slowly to the intended field of gaze. Strabismus associated with limited ductions and diminished saccadic velocity is caused by a rectus muscle paresis, not an oblique muscle palsy.

FIGURE 10-2. Photograph of a child being examined with an optokinetic nystagmus (OKN) drum. The saccadic movement will be in the direction opposite to the drum rotation. This is a good clinical method to estimate if a saccade is present.

movement opposite to the direction of the drum rotation. Compare eye to eye and look for asymmetry of the OKN response. An inability to generate a saccadic movement indicates a paretic rectus muscle.

FORCED DUCTIONS

Forced ductions identify the presence of a mechanical restriction to ocular rotation; these are performed by grasping the eye with a forceps and then passively moving the eye into the field of limited ocular rotation. If the eye shows a resistance to rotation with the forceps (positive forced ductions), then there is a mechanical restriction. When performing forced ductions for possible rectus muscle restriction, proptose the eye to stretch the rectus muscles. This maneuver will allow identification of restriction caused by a tight rectus muscle. If the examiner inadvertently retropulses the eye, the rectus muscles slacken and produce a negative forced-duction test, even if the rectus muscle is tight (Fig. 10-3). The opposite holds true for oblique muscle forced ductions, because retropulsing the eye will stretch the oblique muscles and accentuate a tight oblique muscle. If a restriction is worse with retropulsion of the eye, then the restriction is not caused by a tight rectus muscle but, instead, is

A B

FIGURE 10-3A,B. (A) The proper technique for rectus muscle forced ductions includes grasping the conjunctiva with a 2 3 Lester forceps at the limbus, just anterior to the muscle insertion. First, proptose the eye, and then pull the eye away from the muscle being tested, thus placing the rectus muscle on stretch. This maneuver allows identification of even mildly tight or restricted muscles. (B) The improper technique for rectus muscle forced ductions shows the eye being retropulsed during the maneuver, causing iatrogenic slackening of the muscle and a false-normal forced-ductions test. Positive forced ductions that do not improve when the eye is intentionally retropulsed suggest the presence of a nonrectus muscle restriction, such as periocular scarring (e.g., fat adherence).

secondary to either a periocular adhesion or a tight oblique muscle.

Forced-duction testing can be used as an in-office test using topical anesthesia, or at the time of strabismus surgery. In most cases, the pattern of the eye movements, including the clinical evaluation for saccades, establishes the diagnosis of restriction or paresis. Therefore, in-office forced-duction testing is usually not necessary. If surgery is indicated, forcedduction testing can be performed at the time of surgery to verify the diagnosis. It is important to remember that positive forced ductions does not exclude the presence of a coexisting palsy. In fact, most cases of long-standing rectus muscle palsy also have contracture of the antagonist muscle, so forced ductions will be positive. Preoperative evaluation of muscle function by saccadic eye movement

testing or the forced-generation test (see next section) is required to diagnose a rectus muscle palsy.

FORCED-GENERATION TEST

The forced-generation test directly measures active muscle force and is useful for diagnosing a rectus muscle palsy. To perform this test, the eye is topically anesthetized and grasped with forceps; the patient is asked to look into the field of limited rotation. A sterile cotton-tipped applicator can also be used to push against the eye to feel the abduction force, as noted in Chapter 5 (Fig. 5-16A,B). The examiner feels the pull of the muscle against the forceps or cotton-tipped applicator and compares this to the fellow eye or the antagonist muscle. If there is diminished pull from the muscle into the field of limited rotation, then a paresis is present. Forced ductions can be used in conjunction with forced-generation testing. If forced ductions are positive and the force-generation test shows poor muscle function, then the diagnosis is a combination of restriction and paresis.

INTRAOCULAR PRESSURE CHANGE ON EYE MOVEMENT

Another sign of restriction is increased intraocular pressure on attempted duction into the field of limited movements and away from a restriction or tight muscle. Intraocular pressure increases as the eye forcibly attempts to move against the restriction. Patients with thyroid myopathy and strabismus may show increased intraocular pressure when the pressure reading is made with the restricted eye in forced primary position.

LID FISSURE CHANGES ON EYE MOVEMENT

Ocular restriction caused by a tight rectus muscle or a restrictive adhesion to the globe will cause globe retraction and lid fissure narrowing as the agonist rectus muscle attempts to pull the eye away from the restriction [see Duane’s syndrome (Fig. 10-12), later in this chapter]. These movements occur because the eye is restricted from rotating; therefore, the contracting agonist muscle pulls the eye posteriorly and causes globe retraction and lid fissure narrowing. A rectus muscle paresis will cause the opposite: lid fissure widening and relative proptosis. As the patient looks into the field of action of the paretic rectus muscle, the agonist muscle relaxes secondary to the palsy. The antagonist muscle also relaxes because of