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

PARKS THREE-STEP TEST

Marshall Parks in 1958 published the “Three-Step Test” for the diagnosis of cyclovertical muscle palsies.23 This test identifies which muscle is paretic in patients with a hypertropia caused by an isolated vertical rectus muscle or oblique muscle palsy. The three steps are to determine (1) which paretic muscle might be causing the hyperdeviation in primary position, (2) where the hypertropia is greatest, in rightgaze or leftgaze, and (3) on head tilt, which side the hypertropia is greatest: tilt right or tilt left. See Table 9-1 for results of the three-step test for both vertical and oblique muscle palsy.

The first step is to determine which paretic muscle could be causing a hyperdeviation in primary position. A right hyperdeviation, for example, might be caused by a weak depressor muscle of the right eye (i.e., right inferior rectus or right superior oblique) or a weak elevator muscle of the left eye (i.e., left superior rectus or left inferior oblique).

The second step is to determine in which horizontal field of gaze the hypertropia increases. If the hypertropia increases on gaze away from the hypertropic eye, the paretic muscle is the

TABLE 9-1. Responses to the Three-Step Test for All Vertical and Oblique Muscle Palsies.

ipsilateral oblique or contralateral vertical rectus. A hypertropia that increases to the side of the hypertropia is caused by a paretic vertical muscle on the side of the hypertropia or the contralateral vertical rectus muscle, that is, the paretic muscle is a vertical rectus muscle of the abducting eye or an oblique muscle of the adducting eye. For example, a right hyperdeviation that increases in leftgaze could only be caused by a paretic left superior rectus muscle or a paretic right superior oblique muscle.

The third step is based on the Bielschowsky head tilt test as previously described. This last step can be difficult to calculate, so this author uses a trick that he shamelessly calls Wright’s rule. The author states, “I am sure others have used the same trick to simplify the head tilt test, but I like the way it sounds: Wright’s Rule.” Wright’s rule states that if the hyperdeviation increases on head tilt to the same side of the hyperdeviation, then an oblique muscle is paretic. If the hyperdeviation increases to the opposite side of the hyperdeviation, then a vertical rectus muscle is paretic. For example, if the right hyper increases on head tilt to the right (same side as the hyper), then the oblique muscle is paretic; namely, the right superior oblique (SO) or left inferior oblique (IO) muscle. If the right hyper increases on left head tilt (opposite side of the hyper), then it is the vertical rectus muscle that is weak; namely, the left superior rectus (SR) muscle or right inferior rectus (IR) muscle. Example 6 describes characteristics of a right superior oblique paresis.

Example 6. Right Superior Oblique Paresis

Head tilt test: right, RHT 15 PD; left, RHT 4 PD.

PARKS THREE-STEP TEST FOR EXAMPLE 6

Step 1: Right hypertropia

Right IR or SO versus left SR or IO (underacting muscles, right eye vs. left eye).

Step 2: Right hypertropia increases in leftgaze

Left SR or right SO (the muscles with field of action in leftgaze).

Step 3: Right hypertropia increases in head tilt to the right

Right tilt induces intorsion of the right eye and extorsion of left eye. Both the muscles in contention (RSO and LSR) are

intortors, but only the RSO intorts on right tilt. Therefore, the diagnosis is right superior oblique paresis.

or, by Wright’s rule:

Right hyperdeviation increases on right head tilt (same side as the hyper); therefore, it has to be an oblique muscle paresis. As we are down to two choices from step 2, RSO and LSR, the paretic muscle is the right superior oblique.

SHORTCUT TO THE THREE-STEP TEST

Classically, the paretic muscle is determined by the Parks threestep test as just described. In 1967, Helveston13 described combining steps 1 and 2 to make a two-step test.

This author prefers to start with the head tilt test and use Wright’s rule. To know which vertical rectus or oblique muscle is weak, determine in which horizontal gaze the vertical deviation increases, right or left. As an example, a right hypertropia that increases on head tilt to the right and increases on rightgaze has to be caused by an oblique muscle paresis because the tilt is positive to the same side as the hypertropia. Because the right hypertropia increases on rightgaze, in the field of action of the left inferior oblique muscle (not in the field of action of the right superior oblique muscle), the paretic muscle is the left inferior oblique. Using Wright’s rule alone narrows the choices to two muscles: either an oblique or a vertical rectus muscle of each eye. Determining the horizontal gaze where the hypertropia is greatest tells us which eye, the right eye or the left eye.

PROBLEMS WITH THE HEAD TILT TEST

A positive head tilt test is not infallible when diagnosing cyclovertical muscle paresis. Patients with dissociated vertical deviations, as well as some patients with intermittent exotropia, show a positive head tilt. In addition, the head tilt test is designed to diagnose an isolated paretic muscle, and it may not be reliable when multiple muscles are paretic or if an ocular restriction is present.

Superior Oblique Paresis

A superior oblique paresis is the most common cause for an isolated vertical deviation. The typical findings of a unilateral superior oblique paresis include an ipsilateral hypertropia that increases on contralateral side-gaze and a positive head tilt test with the hyperdeviation increasing on head tilt to the ipsilateral

FIGURE 9-5. Composite nine-gaze photograph of patient with bilateral traumatic superior oblique palsy. Patient has a small esotropia and extorsion in primary position that increases in downgaze. Note the V-pattern (arrow pattern subtype) with a large esotropia in downgaze. There is also severe underaction of both superior oblique muscles associated with relatively mild inferior oblique overaction.

Bilateral superior oblique paresis is associated with bilateral superior oblique underaction, a V-pattern (arrow subtype), little or no hypertropia, and a right hypertropia in leftgaze and a left hypertropia in rightgaze (Fig. 9-5). Other signs include a bilateral extorsion (total greater than 10°), a reversing head tilt test with a right hypertropia in tilt right, and a left hypertropia in tilt left. The presence of an arrow pattern with extorsion increasing in downgaze (Example 7) is diagnostic for an acute bilateral superior oblique palsy and is often seen with traumatic superior oblique palsies. Clinical signs of unilateral versus bilateral superior oblique paresis are shown in Table 9-2.

Example 7. Bilateral Superior Oblique Paresis

Bilateral Maddox Rod—15° Extorsion.

Bilateral extorsion on fundus exam.

Head tilt test: right, RHT 10 PD; left, LHT 10 PD.

ET on downgaze

A bilateral asymmetrical superior oblique paresis can look like a unilateral superior oblique paresis; this is termed masked bilateral superior oblique paresis.16,17 Suspect a masked bilateral paresis if the hypertropia precipitously diminishes in lateral gaze toward the side of the obvious paretic superior oblique muscle and if there is even slight inferior oblique overaction of the fellow eye (see Example 8).

Example 8. Masked Bilateral Superior Oblique Paresis

Head tilt test: right, RHT 25 PD; left, RHT 3 PD.

The presence of a V-pattern and bilateral extorsion on fundus examination also suggest bilateral involvement in patients with a presumed unilateral paresis. In these cases of masked bilateral superior oblique paresis, if surgery is performed only for a unilateral superior oblique palsy, the contralateral superior oblique paresis will become evident postoperatively.

FALLEN EYE

Significant underaction of the superior oblique muscle and fixation with the paretic eye will produce the classic finding called the fallen eye. When a patient with a superior oblique paresis fixes with the paretic eye and tries to look into the field of action of the paretic superior oblique muscle, the weak superior oblique muscle requires a large amount of innervation to make the eye

FIGURE 9-6. Photograph of a traumatic right superior oblique palsy, showing the fallen eye, left eye. The right eye is fixing in the field of action of its paretic superior oblique muscle (i.e., down and in adduction), requiring a great deal of innervation. Because of Hering’s law of equal innervation of yoke muscles, the left inferior rectus muscle (yoke muscle to the paretic right superior oblique muscle) also receives a great deal of innervation. Because the left inferior rectus is at full strength, it overacts and pulls the left eye down, thus causing the appearance of a left fallen eye.

move down and nasally. Because of Hering’s law, the yoke muscle (contralateral inferior rectus muscle) receives an equally large amount of innervation. Because the contralateral inferior rectus muscle has normal function, this increased innervation produces a large secondary hypotropia, or the fallen eye (Fig. 9-6).

INHIBITIONAL PALSY OF THE CONTRALATERAL ANTAGONIST

Chavasse, in 1939, described the term inhibitional palsy of the contralateral antagonist. This term relates to a patient who chronically fixates with the paretic eye, resulting in an apparent weakness on version testing of the yoke muscle to the antagonist of the paretic eye. That is, the paretic eye moves easily into the field of its antagonist with little innervation because the agonist is weak. The yoke muscle to the antagonist of the paretic muscle receives the same small innervation (Hering’s law), so it

will appear paretic on versions because its antagonist is innervated. Clinically, this is seen in association with a congenital fourth nerve palsy and ipsilateral inferior oblique overaction when the patient fixates with the paretic eye. For example, a left fourth nerve palsy with left inferior oblique overaction will produce a left hypertropia increasing in rightgaze. If the patient fixates with the left eye, the innervation required for the left eye to look up and right is minimal, as it is in the field of the overacting left inferior oblique muscle. The yoke muscle to the left inferior oblique muscle is the right superior rectus muscle, and it too will receive little innervation. The right superior rectus will appear to underact or be paretic because its antagonist, the right inferior rectus, is normally innervated and holds the eye down. Inhibitional palsy of the contralateral antagonist is only seen on version testing when the paretic eye is fixing.

PRIMARY INFERIOR OBLIQUE OVERACTION VERSUS SUPERIOR OBLIQUE PALSY

Primary inferior oblique overaction can be differentiated from superior oblique palsy by the head tilt test and type of V-pattern (Table 9-3).

Traumatic Superior Oblique Paresis

Traumatic superior oblique paresis is usually associated with severe closed head trauma, loss of consciousness, and cerebral concussion; however, even very mild head trauma without loss of consciousness can cause a superior oblique paresis. Traumatic superior oblique paresis occurs when the tentorium traumatizes

TABLE 9-3. Primary Inferior Oblique Overaction Versus Superior

Oblique Paresis.

the trochlear nerves as they exit the posterior midbrain posteriorly. Since the two trochlear nerves exit the midbrain together, only a few millimeters apart, the nerve trauma is almost always bilateral. Thus, most cases of traumatic superior oblique paresis are bilateral, although the paresis may be asymmetrical.

The pattern of strabismus is classically, minimal or no hypertropia in primary position, a left hypertropia in rightgaze, a right hypertropia in leftgaze, underaction of both superior oblique muscles, and an esotropia in downgaze (Figs. 9-5, 9-6). There is a positive head tilt with a right hypertropia on right tilt and a left hypertropia on left tilt. Extorsion increasing in downgaze can be demonstrated by Maddox rod and indirect ophthalmoscopy. Patients complain of horizontal or vertical torsional diplopia that is worse in downgaze (Fig. 9-5). In most cases, there is not much ipsilateral inferior oblique muscle overaction, usually 1 or less. Because the strabismus is acquired, patients complain of diplopia—torsional, vertical, and horizon- tal—that increases in downgaze.

The management of traumatic superior oblique paresis is discussed later in this chapter under Treatment of Superior Oblique Paresis.

Congenital Superior Oblique Paresis

The cause of congenital superior oblique paresis is usually unknown. The paresis may be associated with a lax superior oblique tendon or rarely an absent tendon.12 Most cases present as a unilateral paresis or an asymmetrical masked bilateral paresis. Typically, there is a large hypertropia in primary position and significant inferior oblique overaction, usually with relatively little superior oblique underaction (see Fig. 9-4). The most common presenting sign is a head tilt opposite to the side of the palsy. Even though the paresis is present at birth, symptoms often occur in late childhood or even adulthood. It is common for patients to be diagnosed for the first time in middle age. Normally vertical fusional amplitudes are weak and even small acquired hyperdeviations of 3 to 5 PD cannot be fused and result in constant diplopia. Patients with congenital superior oblique paresis, however, develop large vertical fusional amplitudes, and fuse large hypertropias up to 35 PD. The presence of large vertical fusion amplitudes is an important clinical sign that the hyperdeviation is long-standing, rather than acutely acquired, and is suggestive of a congenital superior oblique palsy.