Primary overaction of the inferior oblique muscle apparently is not congenital. Rarely can the onset of this condition be recorded before 1 year of age. More commonly, onset is after 1 year of age; this condition may appear at any time during the first several years, most frequently between 2 and 4 years of age.

Primary overaction of the inferior oblique muscle may be an isolated motility disorder or it may occur in conjunction with a horizontal deviation of the eyes. It seems to occur with equal frequency in patients with esotropia and in patients with exotropia. It appears with equal frequency in patients with congenital esotropia and in those with acquired esotropia. Furthermore, intermittency of the horizontal deviation does not seem to influence the frequency of this disorder. It occurs with about equal frequency in patients with intermittent exotropia and in those with constant exotropia.

Wilson and Parks⁶ performed a statistical analysis of the onset and natural history of primary inferior oblique overaction in 456 strabismus patients. With 5 or more years of follow-up, 72% of patients with congenital esotropia, 34% of patients with accommodative esotropia, and 32% of patients with intermittent exotropia developed inferior oblique overaction at an average age of 3, 6, and 5.2 years, respectively. There was a positive correlation to the number of horizontal surgeries in congenital esotropia but not in the other groups. The incidence of overactive inferior oblique muscles was not related to the age at onset of strabismus, time from onset of strabismus to surgery, age at first surgery, or decompensation of ocular alignment.

Primary overaction of the inferior oblique muscle may have its onset equally in the two eyes or it may occur only in one eye. After developing in one eye, it may gradually develop in the opposite eye. The dissimilarity in the degree of the overaction of the inferior oblique muscles may be temporary; with time, the degrees of overaction in the two muscles may gradually become equal. Unilateral overaction of the inferior oblique muscle occurs with sufficient frequency that the clinician is unable to make the statement that if one inferior oblique muscle overacts, eventually both will overact. In patients with unilateral overactive inferior oblique muscles, Raab and Costenbader⁷ found that the normal second inferior oblique muscle developed significant overaction in about a third of cases after unilateral inferior oblique weakening. In the presence of even the slightest overaction in the nonoperated inferior oblique, unilateral weakening of the overactive inferior oblique was followed in two thirds of cases by worsening of the nonoperated inferior oblique by 2 to 6 months postoperatively. Overaction of the second inferior oblique usually begins within 2 to 6 months of the onset of overaction of the first inferior oblique muscle, whether or not inferior oblique weakening surgery was performed on the eye with the more prominent overactive inferior oblique.

Primary overactions of the inferior oblique muscles that are unassociated with any horizontal deviation of the eyes do not disturb the single binocular vision in the primary position. Depending on the degree of overaction, there is a measurable midline zone of varying size within which the eyes may make horizontal excursions and not disturb the binocular vision. The maximal horizontal excursion that is possible before the gradually increasing vertical phoria transforms to vertical tropia is recorded as the fusion breakpoint, however. At this point, diplopia is encountered. The patient usually responds by subconsciously limiting the horizontal movement of the eyes to the extent that diplopia is avoided. Consequently, on viewing sideways, the patient is more apt to turn the head toward the position desired for seeing than to turn the eyes, except when startled by a visual or auditory stimulus located off to the side beyond the diplopic threshold.

Primary overactions of the inferior oblique muscles associated with a horizontal deviation are one of the mysteries of motility. It is often stated that the longer the duration of the horizontal deviation the greater the tendency for oblique muscle dysfunction. The congenitally esotropic infant, however, who at a young age had excellent surgical correction of the horizontal deviation has the same chance of developing overaction of the inferior oblique muscles some years after the surgery as the congenitally esotropic patient who receives no surgery to correct the horizontal deviation until adulthood. Early corrective surgery for congenital esotropia does not diminish the chance that the congenital esotrope will develop overacting inferior oblique muscles. According to the one study,⁸ about 65% of congenitally esotropic patients are destined to develop overacting inferior oblique muscles. Hiles and coworkers⁹ reported a 78% incidence of inferior oblique overaction in one or both inferior oblique muscles during their study of 54 patients with congenital esotropia. Similarly, elimination of intermittent exotropia at a young age does not preclude future development of primary overacting inferior oblique muscles. Correction of the accommodative esotropia soon after onset with spectacles does not lessen the chance for later development of primary overacting inferior oblique muscles. Therefore, one should question the statement that the longer the duration of the horizontal deviation, the greater the chance of oblique muscle dysfunction.

Weakley and coworkers¹⁰ studied 368 patients with infantile esotropia, acquired accommodative or partially accommodative esotropia, or acquired nonaccommodative esotropia. Of the 126 patients (34%) with amblyopia, 93 patients (74%) had symmetric inferior oblique overaction; however, 31 patients (25%) had more inferior oblique overaction in the eye with the amblyopia. The authors stress that asymmetric inferior oblique overaction in esotropia correlates highly with amblyopia in the eye with greater inferior oblique overaction, regardless of the subtype or duration of the esotropia or the angle of deviation.

Eustis and Nussdorf¹¹ photographed the posterior pole at the time of surgery in 27 eyes of 14 patients with infantile esoptropia. A masked observer graded each photograph for the presence or absence of fundus torsion. Of the 27 eyes, 15 developed inferior oblique overaction and 6 of the 15 demonstrated fundus excyclotorsion before the inferior oblique overaction was clinically recognized. Therefore, the presence of fundus torsion with infantile esotropia may serve as a marker or predictor of subsequent overt inferior oblique overaction.

Primary overaction of the inferior oblique muscles is frequently associated with a V pattern. In patients with congenital esotropia, the overacting inferior oblique muscles are usually associated with dissociated vertical deviation or hypertropia. In some patients, the differentiation between overaction of the inferior oblique muscles and dissociated vertical deviation is difficult. When the eyes are horizontally deviated to the extent that the visual axis of the adducted eye is interrupted by the nose, the eye deviates upward. This can simulate overaction of the inferior oblique muscle to the extent that in some patients it is impossible to make the differentiation.

The treatment of an overacting inferior oblique muscle is to weaken it surgically. Primary overaction of the inferior oblique muscle is not associated with an excyclodeviation, and weakening this primarily overacting muscle does not produce an incyclodeviation. Likewise, primary overaction of the inferior oblique muscle does not produce a significant vertical deviation in the primary position, and surgically weakening this primarily overacting muscle does not produce a vertical deviation in the primary position. Furthermore, unilateral primary overaction of the inferior oblique muscle is not associated with a positive Bielschowsky head tilt test, and this muscle does not produce a positive Bielschowsky head tilt test after the weakening procedure. In all of these respects, the primarily overacting inferior oblique muscle differs from the secondarily overacting inferior oblique muscle. The V pattern that may be associated with overacting inferior oblique muscles is improved by weakening these muscles, particularly between primary position and upgaze.

The inferior oblique muscles have a supposedly secondary abduction action when they contract to move the eyes from the primary position. For many years, allowances were made for a change in the horizontal alignment when the inferior oblique muscles were weakened. The exodeviation was claimed to be improved by 5Δ to 10Δ, and the esodeviation was worsened by 5Δ to 10Δ in patients in whom the primary overacting inferior oblique muscles were weakened. Stager and Parks¹² have proved this claim to be erroneous. In effect, there is no significant change in the horizontal alignment of the eyes produced in the primary position by weakening procedures on primary overacting inferior oblique muscles.

In a prospective study, Parks¹³ investigated the various weakening procedures of the inferior oblique muscles and concluded that the recession procedure was the superior method. As early as 1947, Fink¹⁴ advocated surgery at the origin rather than the insertion of the inferior oblique muscle because of the ease of the approach and the nature of the anatomy and because the degree of effect was more readily controlled when approached at the inferior oblique insertion. The poorest method of inferior oblique weakening is a myectomy between the origin and the nasal border of the inferior oblique muscle. This technique is inadequate because of the significant recurrence of the overacting inferior oblique muscle, which required secondary surgery in 32% of the patients. Three types of surgical weakening procedures were performed on the insertional portion of the inferior oblique muscle temporal to the inferior rectus muscle: (1) recession; (2) disinsertion, allowing the muscle to seek its own insertional site; and (3) myectomy between the temporal border of the inferior rectus and the muscle insertion. Disinsertion has been advocated as an effective, reliable, safe, and fast procedure.^15,16 Parks,¹³ however, found that a tendency for recurrence of the overaction of the surgically weakened insertion end of the inferior oblique muscle was greatest with disinsertion, whereas the result of myectomy was between those produced by disinsertion and recession. Repeat surgery disclosed that the disinserted or myectomized muscle had reattached to the original insertion site in most patients.

Internal ophthalmoplegia of months to years in duration after inferior oblique myectomy has been reported.^17,18 Careful surgical dissection has revealed that the easiest way to locate the ciliary ganglion is to first locate the nerve to the inferior oblique muscle that runs parallel and close to the lateral border of the inferior rectus muscle and to follow it backward to the motor root of the ciliary ganglion.¹⁹ Internal ophthalmoplegia should also be a rare occurrence with recession or denervation and extirpation of the inferior oblique, although this complication has yet to be reported in the literature.

The worst complication occurring in patients whose overacting inferior oblique muscles are weakened is the adhesive syndrome.¹³ This syndrome is manifest by gradual development of hypotropia in the primary position in a patient without vertical deviation before surgery on the inferior oblique muscle.

The hypotropia gradually increases over a period of several months to several years and produces as much as 35Δ of vertical deviation. Furthermore, the patient is unable to elevate the hypotropic eye, and the traction test is positive for resistance to elevation of this eye. On surgical exploration of the hypotropic eye, the inferior oblique is not found to be the cause. Instead, it is Tenon’s capsule in the inferior temporal region, which is thickened by fibrofatty proliferation and scarring to the sclera. This fibrofatty tissue extends to the temporal side of the capsule of the inferior rectus muscle and is attached firmly to the muscle near its insertion. Presumably, cicatrization of the fibrofatty tissue, extending between the tissue of the inferior temporal fornix and the insertional temporal end of the inferior rectus muscle, gradually drags the involved eye farther and farther downward, causing the increasing hypotropia and diminishing active and passive elevation that are particularly obvious in abduction.

Surgical improvement of the adhesive syndrome is difficult; this disorder invariably requires secondary surgery on vertical rectus muscles after the liberation of the involved inferior rectus from scarred Tenon’s tissue and surrounding attachment of this muscle to the sclera. The adhesive syndrome is not related to a particular surgical procedure, as was originally thought when the adhesive syndrome resulting from inferior oblique surgery was described.¹³ Parks encountered it in 13% of the insertional myectomies, 2% of the disinsertions, and none of the recessions or myectomies between the origin of the muscle and the inferior rectus. But additional information revealed the true cause to be a violation of Tenon’s capsule during the dissection of the muscle along its posterolateral border. A tear in Tenon’s capsule results in scarring of the septae within the extraconal fat pad to the sclera and muscle capsules in the inferotemporal sub-Tenon’s space.²⁰

The surgeon performing the weakening procedure should possess adequate skill and knowledge of technique and anatomy to make certain that the entire muscle is dissected and that Tenon’s capsule, containing the intramuscular fat pad, is not opened. Adequate view of the entire insertion can be easily achieved with a sustained adducted and elevated positioning of the eye; this is easily accomplished with a 4-0 silk-stay suture under the lateral rectus muscle attached to the drapes with hemostats. Exposure with a Desmarres or a Conway lid retractor over the insertional site of the inferior oblique is possible through an incision in the inferior temporal fornix; this allows the surgeon to lift the inferior oblique muscle out of its bed near its insertion by direct visualization rather than blindly sweeping a muscle hook under Tenon’s capsule. The blind sweeping procedure has resulted in inadvertent myotomy and myectomy of both the lateral rectus and the inferior rectus muscles. Therefore, elevation of the inferior oblique muscle under direct vision, observation of the total insertion of the muscle, and weakening of the muscle produce significant improvement and do not harm the patient’s eye alignment in the primary position.