Summary
Dysfunction of the inferior oblique (IO) extraocular muscle, whether underaction or overaction, can be remedied with proper examination, diagnosis, and surgical planning and technique. IO overaction is a common component of new and recurring strabismus. Once properly diagnosed through detailed clinical evaluation, IO dysfunction can be corrected with a variety of specific surgical procedures. Familiarity with the surgical anatomy of the IO is required when considering and performing extraocular muscle surgery on the muscle. Knowledge of surgical principles and complications of IO muscle surgery is essential when considering IO surgical treatment.
8 The Inferior Oblique—Strabismus Diagnosis and Surgical Planning: Surgical Anatomy, Surgical Principles, and Wound Healing
8.1 History/Background
Reports of surgery on the inferior oblique (IO) muscle date back to the mid-19th century. The first description comes from Bonnet’s 1 tenotomy of the IO muscle for the treatment of high myopia and asthenopia in 1841. Later in the century, surgeons began exploring IO weakening surgery as a treatment for torticollis. 2 , 3 , 4 At the time, IO weakening was also recommended in superior oblique (SO) paralysis, inferior rectus (IR) paralysis, and progressive or malignant myopia. 5 In 1898, the popular opinion regarding the direct operation on the IO was that it should be generally avoided at all costs. 6 In the early 20th century, surgeons became interested in tenotomy of the IO as first successfully reported by Duane in 1906. 7
Prior to 1935, surgery to weaken the IO was directed at its origin, rather than its insertion. White and Brown 8 first recommended tenotomy, disinsertion, and myotomy of the IO at the insertional end of the muscle. At the time, these techniques proved unpopular due to unsatisfactory results. 9 In the 1960s, many surgeons 10 , 11 , 12 popularized recession, disinsertion, and myotomy at the insertion or middle of the IO. In 1972, Parks 13 evaluated four different weakening operations in a controlled study and concluded that the recession operation was the most effective and long lasting. Apt and Call 14 carefully chronicled the anatomical position of the IO muscle in 200 consecutive autopsy eyes, providing information for locating the exact point on the globe for the desired amount of recession. Fig. 8‑1 details these measurements by converting cord lengths to circumferential distances. The magnitude of recession has differed among surgeons due to the use of different landmarks from which surgical reattachment position is measured.
By the end of the 20th century, it was possible to predict the effects of anterior and anterior nasal transposition on the change in the direction of the torque vector, allowing consistent treatment of excyclotorsion using the IO. 15 A variety of procedures for weakening the IO muscle are now practiced, most of which have their origins in the early 20th century. There were many procedures proposed for IO underaction, but unsatisfactory results caused their abandonment. Today, treatment of underacting IO muscles is generally directed at the antagonist or contralateral yoke muscle. 5
8.2 Clinical Presentation
8.2.1 Inferior Oblique Weakness or Underaction
Historically, IO underaction (“palsy”) is the least commonly seen isolated muscle weakness. 16 , 17 The prevalence and incidence of IO palsy is unknown. It may affect patients of any age, sex, or race. Patients present with a vertical deviation, commonly in association with diplopia, head tilt to the side of the palsy, and/or face turn away from the side of palsy. The hypertropia is greater in side gaze. The palsy can be primary or secondary, as well as unilateral or bilateral. Patients may present with hypertropia on the side opposite that of the palsy. Similarly to Brown’s syndrome, elevation is deficient in the adducted position of the eye.
Editor’s Comment
Pulley displacements and flap tear–related restrictions often simulate muscle underactions and “palsies.” It would be difficult to anatomically explain an isolated nerve palsy to a small branch of the third cranial nerve to just the IO. When confronted with the situation of underelevation of the eye, greater in adduction, the reader should consider these other “masquerade” etiologies (Chapter 4, Chapter 19, Chapter 20).
8.2.2 Inferior Oblique Overaction
Overaction (or apparent overaction) of the IO is a common aspect of new and recurring cases of strabismus. IO overaction is described as overelevation in adduction in A Classification of Eye Movement Abnormalities and Strabismus (CEMAS) and by others. 18 , 19 This overaction can be primary or secondary. Primary IO overaction indicates no association with SO or superior rectus (SR) paresis or palsy. When the overaction is associated with other muscle paresis or palsy, the term secondary is used. Primary IO overaction commonly develops in individuals with infantile esotropia (often after surgical treatment of the original strabismus), accommodative esotropia, and intermittent exotropia. It is also frequently associated with dissociated vertical deviation (DVD). IO overaction associated with SO weakness is one of the most common causes of vertical strabismus in adults. 20 Wilson and Parks estimated the incidence of IO overaction to be 72% among individuals with infantile esotropia and greater than 30% among those with acquired esotropia or intermittent exotropia. 21 Primary IO overaction has been reported to represent 16.7% of childhood hypertropias. 22 IO overaction can be unilateral or bilateral, which may be asymmetrical due to differences in onset or severity. Patients present with recent or recurrent onset, typically with prior strabismus involving other extraocular muscles. Patients may have a head tilt, diplopia, and/or a vertical deviation in side gaze.
8.3 Clinical Evaluation and Diagnosis
IO dysfunction can be manifest by either underaction or overaction of the muscle. The dysfunction is usually best seen in supraduction during maximum adduction. Most observers grade underaction or overaction by the amount of hypotropia or hypertropia of the adducting eye during supraduction while versions are performed. The most popular grading system is based on the subjective assessment of hypotropia or hypertropia when compared to the contralateral abducting eye. Roughly, a hypotropia or hypertropia of 7 degrees is designated as –1 or +1; 14 degrees, –2 or +2; 21 degrees, –3 or +3; and 28 degrees, –4 or +4 underaction or overaction of the IO. Quantification of the inferior oblique underaction or overaction magnitude varies dramatically from one strabismologist to another, even in the same patient tested at the same time. Subjective assessments are fraught with many difficulties due to interpatient differences such as large epicanthal folds, ptosis, abnormal lid elevation, and mongoloid lid folds.
8.3.1 Inferior Oblique Underaction
Three key features confirm IO underaction upon examination. First, the vertical deviation worsens with gaze and tilt away from the affected eye. Second, there is impaired elevation of the affected eye in adduction. Third, no restriction in forced duction to elevation in adduction is seen. Brown’s syndrome, which can mimic IO underaction, is differentiated by restrictive forced duction to elevation, A-pattern strabismus, and SO overaction. Pulley heterotopias may also simulate IO underaction. Nonsurgical management includes treating any associated illnesses and use of prisms. Surgical management consists of either ipsilateral SO or contralateral SR weakening. The aim of surgery is to eradicate abnormal head position, diplopia, and any noticeable vertical deviation.
8.3.2 Inferior Oblique Overaction
Primary IO overaction generally produces a vertically incomitant V-pattern strabismus. With the eyes in lateral gaze, alternate cover testing shows that the higher (adducting) eye refixates downward and the lower eye refixates with an upward movement. A difference of 15 to 20 prism diopters in horizontal deviation between 30-degree upgaze and 30-degree downgaze is generally considered significant enough to consider an IO weakening surgery. 5 The appearance of IO overaction (overelevation in adduction) may be mimicked by abnormal function of other extraocular muscles, such as in SO weakness, cocontraction of the horizontal rectus muscles, aberrant innervation of the extraocular muscles, anomalies of the extraocular muscle insertion, 23 or pulley heterotopia (Chapter 4, Chapter 19).
In small children and infants with concurrent IO overaction and large infantile esotropia, it can be difficult to obtain fixation with the abducting eye in order to identify the overaction in the contralateral eye. In these cases, the principal evidence of overaction in the adducting eye may be a hypotropia of the abducting eye. This may only be seen if sufficient abduction can be obtained, often not an easy task in infantile esotropia with equal vision and cross fixation. If fixation preference for one eye is present, abduction to that side will generally be more complete and identification of the IO overaction in the contralateral eye may be possible. The presence and severity of amblyopia can affect the degree of overaction. It is common to find a significantly greater IO overaction on the side of the amblyopic eye. 24
With IO overaction, the hypertropia of the adducting eye may initially manifest during different phases of version testing. Our recommendation is to not only grade the degree of vertical tropia on a scale of 1 to 4, but also observe and record the initial types of horizontal presentation and the presence and degree of abnormal abduction during maximum supraduction in adduction (V pattern). 25 These observations should be noted both preoperatively and postoperatively.
A latent DVD may manifest due to occlusion of the visual axis by the nasal bridge in extreme adduction and mimic IO overaction. This can be distinguished from actual overaction by forcing fixation with the adducting and supraducting eye just short of occlusion of its visual axis by the nasal bridge and looking for a true DVD of the contralateral abducting eye. Because DVD and IO overaction may occur simultaneously and appear similar upon examination, it is important to be able to distinguish the true cause of the hypertropia. Measuring the hypertropic refixation movement in the contralateral eye by prism cover test reveals the true hypertropic component. After measuring the total upward drift by prism under cover test, the difference between the two measurements constitutes the component caused by the DVD. 26
Another method of assessing IO dysfunction is by exaggerated forced duction testing. 27 This is useful to mechanically assess the tightness of the IO pre- and postoperatively. Three methods of forced duction are frequently utilized. The limbus can be grasped with forceps temporally and the eye can be rotated nasally. One can then differentiate nonrestrictive underaction from restrictive underaction seen in Brown’s syndrome by passively depressing or elevating the eye to detect any resistance to rotation. Exaggerated forced ductions allow for a more successful assessment of the degree of IO tightness. The perilimbal conjunctiva should be grasped at the 3 o’clock and 9 o’clock positions and the globe posteriorly displaced into the orbit. With the eye infraducted, it is rotated from an abducted to an adducted position. The IO will become taut and its tension can be felt and evaluated as the muscle slips over the posterior pole of the globe. If during surgery the IO demonstrates tightness before weakening, repeat postweakening forced duction testing can confirm that all muscle and tendon fibers have been incised, reducing the possibility of a residual overaction. Torsional forced duction can also be helpful (Chapter 3, Chapter 9, Chapter 11).
As a consequence of SO palsy, unilateral IO overaction (secondary) can be treated with surgical weakening of the IO. Diagnosing unilateral inferior oblique overaction must be done with caution. Initially, the overaction in the fellow eye may only become evident after the obviously overacting IO is weakened. 28 Full sensorimotor examination with detailed measurements is required in straight ahead, left, right, and tilted head positions. Determining whether the IO overaction is associated with diplopia or suppression without diplopia will allow the physician to best decide on necessary management.
8.4 Surgical Anatomy
A complete understanding of the anatomy of the IO is essential to anyone attempting surgery on this muscle. The IO is anatomically unique. It is the only extraocular muscle that does not originate at the apex of the orbit. The IO is approximately 37 mm in length. As it passes from its insertion, it forms a 51-degree angle with the visual axis of the eye (in primary position). This accounts for its primary excyclotorsion effect. The posterior relation of the insertion to the origin results in the elevating effect of the IO.
The origin, located just behind the inferior nasal orbital rim on the periosteum of the maxillary bone, is tendinous, attaching to the periosteum on an area approximately 3.0 by 1.5 mm. There is no blood supply in this portion that extends for only the first 3 to 4 mm of muscle length. When the IO is cut in this area, bleeding will occur from the temporal but not the nasal side of the incision.
As the muscle passes temporally and posteriorly toward its insertion, it is wrapped in extraconal fat until penetrating Tenon’s capsule approximately 8 to 10 mm distal to its origin. Nasal to the IR, the IO muscle is oval and approximately 2 to 5 mm in diameter. When stretched between two muscle hooks, the nasal portion of the IO usually shows a “notch” where the narrow portion of the IO sharply widens as it passes temporally. The posterior muscle border then angles toward the orbital apex, and the anteroposterior diameter increases to 8 to 10 mm as it passes beneath the IR. The neurofibrovascular bundle (NFVB) enters near the posterior border of the IO. The NFVB contains the motor nerve of the IO, a branch of the inferior division of the oculomotor nerve, and a muscular branch of the ophthalmic artery that provides blood supply to the muscle. The anterior border of the IO is 5 mm posterior to the main insertion of the IR. This relationship is important in understanding the mechanics of anterior transposition surgery.
Fibrous bands adjacent and nasal to the NFVB extend posteriorly from the capsule of the IO to the capsule of the IR 17 to 22 mm posterior to the IR insertion. The fibrous bands, with the NFVB, serve as an ancillary origin for the posterior fibers of the IO muscle at the myoneural junction. 29 Cadaver dissections, microscopic studies, and elastic modulus studies have revealed that the NFVB and its surrounding fibrous tissue bands represent a very taut structure, which acts as an inelastic cord that tethers the midportion of the IO to the posterior orbit. 15 When the IR is recessed, these fibrous attachments between the IO, IR, and lower lid can cause retraction of the lower lid unless they are lysed for 20 to 25 mm posterior to the IR insertion. Suturing the IO capsule anteriorly to the IR or sclera at a distance from the limbus equivalent to their original location can also be helpful in preventing lower lid retraction.
The IO is the most vascular at its midportion. Incision into the muscle in this area, as occurs during myotomies and myectomies, can produce severe hemorrhaging that may result in fibrosis and a secondary hypotropia. Thus, good hemostasis is essential during surgery in this area. From the level of the NFVB, the IO proceeds temporally to its insertion beneath the inferior border of the lateral rectus (LR) muscle near the macula. The location varies but usually is 10 to 12 mm posterior to the inferior edge of the LR insertion. Its insertion narrows to a 1-mm thickness and there is little or no tendinous portion. It is important to recognize the close approximation of the insertion of the IO to the LR when dissecting and take care to avoid iatrogenic damage to the LR.
Near its insertion, the posterior edge of the IO lies on the inner surface of the posterior Tenon’s capsule, which separates the muscle and the globe from extraconal fat tissue. Between the inferior and lateral rectus muscles, the intermuscular septum along the posterior edge of the IO extends only 2 mm before fusing with the posterior Tenon’s capsule. This is the most common site of isolating the IO, and this anatomical relationship must be clearly understood and remembered during IO surgery. Dissection along the posterior border of the IO must be very close to the muscle edge; otherwise, Tenon’s capsule may be violated, causing intraconal fat to enter the sub-Tenon’s space and adhere to the sclera. The resultant cicatricial effect can produce severe restrictive hypotropia.
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