Left, Orientation of muscles at the time of transposition. The lateral rectus (LR) muscle insertion is positioned just lateral to the lateral border of the inferior rectus (IR) muscle insertion, with the new insertion parallel to the spiral of Tillaux, with the original distance A equal to A‘. The superior rectus (SR) muscle is oriented in a similar manner just superior to the medial rectus (MR) muscle insertion, with the original distance B equal to B‘. A superior oblique (SO) tenotomy is carried out with the gap between the cut ends bridged by a nonabsorbable suture. Right, Modification of the surgical procedure if the lateral rectus muscle has been previously recessed. The new position of the lateral rectus muscle insertion is just lateral to the lateral border of the inferior rectus muscle. The new insertion of the lateral rectus muscle is parallel to the spiral of Tillaux. The distance of the new insertion from limbus is not changed (A=A‘).
Ocular motility of patient 1 at 25 years of age, just before undergoing the second surgical procedure.
Diplopia-free field of patient 1 tested on the same day as Figure 1 was obtained.
Ocular motility of patient 1 at 30 years of age, 5 years after the patient underwent the surgical procedure recommended by Knapp.7
Diplopia-free field of patient 1, 5 years after the surgical procedure, tested on the same day as Figure 3 was obtained.
Kushner BJ. Surgical Treatment of Paralysis of the Inferior Division of the Oculomotor Nerve. Arch Ophthalmol. 1999;117(4):485-489. doi:10.1001/archopht.117.4.485
Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999
Paralysis of the inferior division of the oculomotor nerve is relatively rare. Little has been written about its surgical treatment.
Five patients with paralysis of the inferior division of the oculomotor nerve were treated with transposition of the superior rectus muscle toward the insertion of the medial rectus muscle, transposition of the lateral rectus muscle toward the insertion of the inferior rectus muscle, and tenotomy of the superior oblique tendon in the affected eye.
All 5 patients had a satisfactory outcome. They were free of diplopia in the primary position as of their last examination. Follow-up ranged from 3 to 10 years after surgery.
Paralysis of the inferior division of the oculomotor nerve can be adequately treated by simultaneous transposition of the superior rectus muscle toward the insertion of the medial rectus muscle, transposition of the lateral rectus muscle toward the insertion of the inferior rectus muscle, and tenotomy of the superior oblique tendon in the affected eye.
THE THIRD cranial nerve provides innervation to the medial rectus muscle, the inferior rectus muscle, the superior rectus muscle, the inferior oblique muscle, the levator palpebrae superioris muscle, the ciliary body, and the sphincter of the pupil. Typically, as it enters the orbit through the lower part of the superior orbital fissure, it divides into a superior branch and an inferior branch; there is, however, some variability in the location of this division. The inferior branch provides innervation to the inferior oblique, the medial rectus, and the inferior rectus muscles. It also innervates the sphincter of the pupil and ciliary body via a branch that passes to the ciliary ganglion. Isolated paralysis of the inferior division of the oculomotor nerve is rare.1- 5 In one large series of patients with oculomotor nerve paralysis, only 1 of the 54 patients described had the involvement isolated to the inferior division.2 In a published round table discussion of the treatment of a patient with paralysis of inferior division of the oculomotor nerve, 5 experienced strabismologists reported very limited experience with that entity. Some had never treated a patient with it, and others had only seen it several times.6
The cause of paralysis of the inferior division of the oculomotor nerve has been reported to be local orbital disease or trauma, viral, ophthalmoplegic migraine, aneurysm, vasculitis, demyelinating disease, or unknown.1- 6 It can also occur after incomplete recovery of a complete acquired oculomotor nerve paralysis. The clinical appearance of a patient with a paralysis of the inferior division of the oculomotor nerve is that of a large exotropia and hypertropia of the affected eye, and usually an internal ophthalmoplegia. Typically the affected eye has intortion.
Little has been written about the surgical management of this entity. Knapp7 briefly described a surgical procedure he found effective for treating this entity; however, specific data and details were not provided. The operation consists of simultaneous transposition of the superior rectus muscle toward the insertion of the medial rectus muscle, transposition of the lateral rectus muscle toward the insertion of the inferior rectus muscle, and tenotomy of the superior oblique tendon in the affected eye. I have used the operation recommended by Knapp in 5 patients and achieved satisfactory results. The purpose of this report is to call attention to the efficacy of Knapp's recommended surgical procedure.
I examined all patients in the series and treated them according to the previously described lines recommended by Knapp.7 At surgery, the superior rectus muscle was sutured just adjacent to the superior border of the insertion of the medial rectus muscle, with the new insertion of the superior rectus muscle following the spiral of Tillaux. Similarly, the lateral rectus muscle was sutured just adjacent to the lateral border of the insertion of the inferior rectus muscle, also following the spiral of Tillaux. For both muscles, the intermuscular septae and check ligaments were cut as far posteriorly as was practical at the time of surgery. In cases in which there was moderate contracture of the superior or lateral rectus muscle, a recession of several millimeters was carried out, depending on intraoperative findings. Also, a tenotomy of the ipsilateral superior oblique tendon was performed just nasal to the nasal edge of the superior rectus muscle. A nonabsorbable suture was used to bridge the gap between the 2 cut ends of the superior oblique tendon as recommended by Knapp (Figure 1). Adjustable sutures were used on the lateral rectus and superior rectus muscles in cases 2 and 4. They each underwent small adjustments of both muscles (approximately 1-2 mm) in the form of increasing recession at the time of adjustment after surgery.
Measurements before and after surgery were all performed with the alternate prism and cover test with appropriate spectacle correction in place. Diplopia-free fields were plotted on the Goldmann perimeter according to the standard method previously described.8 In all cases, paralysis of the muscles was diagnosed by a combination of forced duction and active force generation testing; saccadic velocity testing was not performed.
Case 1 will be described in detail. The others will be presented in tabular form.
I first examined patient 1 when she was 17 years of age. She reported diplopia associated with a left exotropia and hypertropia that she was able to eliminate with a face turn to the right and chin-down head posture. On the basis of medical history and a review of old photographs, the problem had been present at least before 8 years of age. The patient believed the onset had been gradual and insidious. She had also noted anisocoria with a larger pupil in the left eye for the same period. At 13 years of age she had been diagnosed as having type 1 diabetes mellitus.
At the time of my initial examination, she had 30 prism diopters (PD) of left exotropia and 20 PD of left hypertropia in the primary position with −4 underaction of the left medial rectus, left inferior rectus, and left inferior oblique muscles (scale, −4 to +4). Her left pupil was fixed and dilated at 8.0 mm. She had no other neurologic symptoms. A computed tomographic scan of the head and orbits was unremarkable. At the time of that examination, magnetic resonance imaging was not yet available. Further workup for an aneurysm was not carried out because of the age at onset of her symptoms and their chronicity.
I operated on her, performing an 8.0-mm recession of the left lateral rectus muscle and an 8.0-mm resection of the left medial rectus muscle with 1 full tendon width infraplacement of both muscles. This initially improved her alignment in the primary position; however, her deviation rapidly recurred. By 1 year after surgery, her measurements were essentially the same as preoperatively. She was then unavailable for follow-up for 8 years, at which time she returned desiring further surgical correction of her strabismus. She was manifesting a 30-PD left exotropia and a 20-PD left hypertropia. Ductions were essentially the same as before her first surgical procedure. Her ocular motility at 25 years of age is demonstrated in Figure 2. Diplopia-free field testing disclosed a small eccentrically located window of single binocular vision (Figure 3). Magnetic resonance imaging showed multiple small foci of increased signal intensity that were periventricular, in the corpus callosum and in the brain stem. These were considered suggestive of a demyelinating disease, but (at the time) also thought to be consistent with long-standing diabetes mellitus. She had no other neurologic symptoms.
At 25 years of age, the patient underwent the surgical procedure described by Knapp7 to treat paralysis of the inferior division of the oculomotor nerve. Because her left lateral rectus muscle had been previously recessed 8 mm, at the time of her second surgical procedure it was 15 mm from the limbus. Consequently, when the muscle was transposed, the point of reattachment was 15 mm from the limbus and adjacent to the lateral border of the inferior rectus muscle. The new insertion of the muscle was parallel to the spiral of Tillaux (Figure 1). At the time her surgery was performed, the surgical technique of McKeown et al9 to spare the ciliary arteries had not yet been published. After surgery, her eyes were essentially straight and she was free of diplopia in the primary position; she no longer had to assume an abnormal head posture.
Approximately 1 year after this second surgical procedure, she experienced symptoms of dizziness and dysphagia. She was subsequently diagnosed as having multiple sclerosis. Although her multiple sclerosis has been progressive and severe, she has maintained good ocular alignment. When I last examined her 5 years after her second strabismus surgical procedure, she had 4 PD of exophoria and 4 PD of left hyperphoria in the primary position. Her ocular motility as of that examination is shown in Figure 4 and her diplopia-free field in Figure 5. She had no cyclotropia with the double Maddox rod test.
The clinical characteristics of the other 4 patients are presented in Table 1. The various causes of the oculomotor nerve paralyses seen in patients in this series are similar to those in other reports.1- 5 All had troublesome diplopia before surgery and compensated for it either by occluding 1 eye or by assuming a face turn toward the affected eye with a chin-down head posture. Each patient had been documented as having a stable paralysis of the inferior division of the oculomotor nerve for at least 1 year before surgery. In 4 of the patients, the left eye was affected; in case 4 the right eye was affected. To simplify comparison of data analysis, case 4 is presented in the table as though the affected eye were the left eye. All patients underwent central nervous system imaging in the form of either computed tomography or magnetic resonance imaging, depending on the available technology at the time they were treated.
Two of the patients were presbyopic in their nonparetic eye because of age. They both required either separate single-vision reading glasses containing prism, or slab-off prism in their bifocal to be free of diplopia for reading (cases 2 and 4). All of the patients had an internal ophthalmoplegia; however, the 3 patients who were not presbyopic in their nonparetic eye were able to read comfortably at near under binocular conditions without additional plus lenses. They were, in effect, using monovision. Several of them elected to use a miotic in the affected eye on a long-term basis to decrease the photophobia resulting from the internal ophthalmoplegia. All patients showed good stability in their alignment after surgery. None had good adduction or depression of the affected eye. None had a symptomatic cyclotropia in the primary position as measured with the double Maddox rod test.
In addition to patient 1, patient 3 had undergone a previous surgical procedure. It consisted of a 12.0-mm recession of the lateral rectus muscle and a 10.0-mm resection of the medial rectus muscle in the affected eye. Consequently, at the time patient 3 underwent the operation that is the subject of this report, the technique described by McKeown and coworkers9 to spare the anterior ciliary arteries was used. At the time of the transposition procedure, the lateral rectus muscle was found 18 mm from the limbus. The site of reattachment during the transposition was kept at 18 mm from the limbus and was oriented as shown in Figure 1.
None of the patients had a measurable ptosis of the affected eye before surgery. This is what one would expect with a paralysis of the inferior division of the oculomotor nerve. Several patients did show a slight to moderate narrowing of the palpebral fissure after surgery, presumably from the anterior transposition of the superior rectus muscle (Figure 4). Unfortunately, the palpebral fissure was not accurately measured in most cases; no patients noted or complained about ptosis after surgery.
The treatment of paralytic strabismus is difficult. Usually transposition procedures are necessary to obtain a satisfactory result. My own experience with performing a horizontal recession and resection procedure with infraplacement of both horizontal rectus muscles has been disappointing in patients with paralysis of the inferior division of the oculomotor nerve (cases 1 and 2). Knapp7 also found conventional surgery disappointing for treating that entity in both of the patients in whom he attempted it; however, he found the surgical procedure described in this report to be satisfactory in the 3 patients on whom he performed it (P. Knapp, MD, written communication, 1987).
Although transposition of a muscle does not actually create an effective duction in the direction in which the muscle is transposed, it does provide some active force in that direction. This stabilizes the eye and guards against a drift toward undercorrection. Although all 5 patients in this series had substantial limitation of ocular rotation after treatment, they were symptomatically comfortable and greatly improved when compared with their preoperative status. Ideally, a treatment for paralysis of the inferior division of the oculomotor nerve would provide better adduction and depression of the affected eye after surgery. I am not aware of any alternative treatments that have been shown to accomplish this. Possibly with additional surgery on either the affected or unaffected eye, the range of single binocular vision in these 5 patients could be expanded. None has elected to have additional surgery.
It is not surprising that none of the patients had a subjective cyclotropia after surgery. Paralysis of the inferior division of the oculomotor nerve is associated with an abnormal incyclotropia, because the normal superior oblique muscle is unopposed by the paretic inferior oblique muscle. The surgical procedure performed in these patients involved weakening the superior oblique muscle and thus corrected the incyclotropia.
The procedure recommended by Knapp7 appears to be an effective way of treating paralysis of the inferior division of the oculomotor nerve.
Accepted for publication December 1, 1998.
This study was supported by an unrestricted grant from Research to Prevent Blindness Inc, New York, NY, and the Wisconsin Lions Foundation, Stevens Point (to the Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison).
Corresponding author: Burton J. Kushner, MD, University of Wisconsin Hospital and Clinics, 2870 University Ave, Suite 206, Madison, WI 53705 (e-mail: email@example.com).