Journal of Pediatric Ophthalmology and Strabismus

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Iatrogenic Inferior Rectus Palsy

Michael C Brodsky, MD; Katherine J Fritz, CO; Susan H Carney, MD

Abstract

ABSTRACT

We examined two patients who developed unilateral inferior rectus muscle palsy following inferior oblique myectomy. Surgical exploration showed a normal inferior rectus muscle and tendon in both patients. Surgical correction consisted of inferior rectus resection in one patient and inferior rectus resection combined with an ipsilateral superior rectus recession in the other. We propose inadvertent excision of the lateral portion of the inferior rectus muscle during inferior oblique myectomy as the probable mechanism of inferior rectus injury.

Abstract

ABSTRACT

We examined two patients who developed unilateral inferior rectus muscle palsy following inferior oblique myectomy. Surgical exploration showed a normal inferior rectus muscle and tendon in both patients. Surgical correction consisted of inferior rectus resection in one patient and inferior rectus resection combined with an ipsilateral superior rectus recession in the other. We propose inadvertent excision of the lateral portion of the inferior rectus muscle during inferior oblique myectomy as the probable mechanism of inferior rectus injury.

INTRODUCTION

Isolated inferior rectus palsy, once thought to be a rare entity, has been the subject of a number of recent clinical reports.1'3 Documented etiologies include third nerve nuclear lesions,4"6 central nervous system lesions involving the cerebellum or cervicomedullary junction,7 myasthenia gravis,8,9 and orbital injuries.10 Recently, von Noorden and Hansell described a congenital variant of inferior rectus palsy.1

We examined two patients who developed acute, unilateral inferior rectus palsy following ipsilateral inferior oblique myectomy. In this report, we describe their unusual clinical presentations, probable mechanism of inferior rectus injury, and response to surgical treatment. To our knowledge, this is the first description of inferior rectus palsy following strabismus surgery.

CASE REPORTS

Case 1. An 11-year-old girl was referred for evaluation of vertical diplopia following a right inferior oblique myectomy. She had a history of congenital esotropia that was treated with bilateral medial rectus recessions at 1 year of age. Postoperatively, she had good ocular alignment until 8 years of age, when her right eye began "drifting up." Her ophthalmologist diagnosed an overaction of the right inferior oblique muscle and performed a right inferior oblique myectomy. Postoperatively, she noted vertical diplopia and began tilting her head to the right.

On our examination 6 months later, the patient's visual acuity was 20/20 in each eye. Both pupils reacted normally to light and there was no afferent pupillary defect. Results of version testing are shown in Figure 1. There was decreased infraduction of the right eye, worse in the field of action of the inferior rectus muscle. Field measurements showed an ?-pattern with a right hypertropia, worse on right gaze and on left head tilt (Fig 2). The patient reported no torsion on Maddox double rod testing. Results of magnetic resonance imaging of the head and orbits were normal. A Tensilon test was negative.

Six months later, the patient's ocular motility measurements were unchanged. Surgical exploration of the right inferior rectus muscle and tendon revealed no visible abnormality. Intraoperative forced duction testing was negative. A right inferior rectus resection (4 mm) and a right superior rectus recession (6 mm) were performed. Postoperatively, her diplopia was resolved. At the last follow-up examination, 9 months later, she had only a slight right inferior rectus underaction (Fig 3). She had a small residual hyperphoria in primary gaze and developed a right hypertropia only in right gaze and with left head tilt (Fig4X

Case 2. A 79-year-old woman was referred for vertical diplopia in downgaze following inferior oblique myectomy. She had initially noted a gradual onset of vertical diplopia in 1985, at which time her ophthalmologist diagnosed a small left hypertropia as well as early nuclear sclerotic cataracts. The patient was treated with prisms which were ground into her spectacle lenses. She continued to have intermittent vertical diplopia, and her prisms were increased in strength several times over the next 3 years. She was healthy except for rheumatoid arthritis for which she took aspirin. She had been treated with penicillamine 2^2 years previously for a period of 9 months.

By April 1989, her visual acuity had decreased to 20/40 OD and 20/60 OS. She had 10.00 diopters of left hypertropia which increased in right gaze and was diagnosed as having an overaction of the left inferior oblique muscle. She underwent a combined left inferior oblique myectomy and extracapsular cataract extraction with posterior chamber intraocular lens (PC-IOL) implant. In the operative note, the surgeon stated that the lateral and inferior rectus muscles were isolated on large muscle hooks prior to the myectomy. Postoperatively, the patient noted increased vertical diplopia in downgaze.

On our examination in October 1989, corrected visual acuity was 20/25 in the right eye and 20/50 in the left eye. Both pupils reacted normally to light and there was no afferent pupillary defect. Version testing showed marked underaction of the left inferior rectus and superior oblique muscles, and mild underaction of the left inferior oblique muscle. Duction testing showed decreased depression of the left eye in all fields of gaze. Field measurements are summarized in Figure 5- Slit-lamp examination showed an early nuclear sclerotic cataract in the right eye and a PC-IOL in the left eye. Retinal examination was normal. A Tensilon test was negative. A CT scan of the head and orbits was normal.

FIGURE 1: Case 1: Preoperative examination of versions in nine cardinal positions of gaze and right and left head tilt. Note right hypertropia on attempted downgaze, greatest in the field of action of the right inferior rectus muscle. Also note the marked right hypertropia on left head tilt.

FIGURE 1: Case 1: Preoperative examination of versions in nine cardinal positions of gaze and right and left head tilt. Note right hypertropia on attempted downgaze, greatest in the field of action of the right inferior rectus muscle. Also note the marked right hypertropia on left head tilt.

FIGURE 2: Preoperative field measurements. Curved arrows indicate ocular alignment in right and left head tilts.

FIGURE 2: Preoperative field measurements. Curved arrows indicate ocular alignment in right and left head tilts.

In January of 1990, we performed a 4-millimeter left inferior rectus resection. At surgery, the inferior rectus muscle and tendon appeared grossly normal and a forced auction test was negative. Postoperatively, she had no diplopia in primary gaze, but noted residual vertical diplopia in 30" upgaze and downgaze. Six months postoperatively, she was orthophoric in all horizontal fields of gaze, with 10.00 prism diopters of left hypertropia in downgaze and 5.00 prism diopters of right hypertropia in upgaze.

DISCUSSION

Neuroanatomically, there are two sites at which a third nerve injury could produce an isolated paresis of the inferior rectus muscle. One site is the oculomotor nucleus, where cell bodies of neurons destined for their target muscles are each segregated into a distinct subnucleus.3"6 The orbit is a second site where an injury or disease process involving either the inferior rectus muscle, its myoneural junction, or its nerve may result in isolated inferior rectus dysfunction. In this regard, blowout fractures direct muscle injury),10 retrobulbar injection (local myotoxicity),11 and myasthenia gravis (myoneuraljunction disease)8,9 are documented causes of inferior rectus palsy.

We are unaware of previous reports of inferior rectus palsy following strabismus surgery. In both of our patients, the ocular motility findings on our initial examination appeared to conflict with the clinical history. The history of previous unilateral inferior oblique overaction, together with unequivocal findings of ipsilateral inferior rectus palsy, initially led us to speculate that a single disease process such as myasthenia gravis could account for this unusual combination of findings. In our second patient, the history of penicillamine ingestion, which has been associated with myasthenia gravis,12 further suggested this possibility. Indeed, it is possible that penicUlamine ingestion could have contributed to this patient's initial ocular misalignment. Alternatively, sensory dissociation from her cataracts could have allowed a previously controlled hyperphoria to become manifest.11 In both patients, signs and symptoms of acute inferior rectus palsy coincided with inferior obUque myectomy. Their ocular motility findings subsequently remained stable over a 6-month period, further supporting the notion that the inferior rectus muscle was inadvertently injured during strabismus surgery.

We believe that inferior rectus injury in our patients was caused by inadvertent excision of the lateral portion of the inferior rectus muscle located within the fascia! attachments of Lockwood's ligament. During inferior oblique myectomy, the distal portion of the inferior oblique muscle is identified and isolated. The inferior oblique muscle is then clamped distaliy and cut at its insertion to the globe. It is again clamped just temporal to the inferior rectus muscle and cut, to excise the major portion of the inferior oblique muscle distal to the inferior rectus muscle.

FIGURE 3: Case 1: Postoperative examination of versions. Note the improved ocular alignment with no residual right hypertropia in downgaze.

FIGURE 3: Case 1: Postoperative examination of versions. Note the improved ocular alignment with no residual right hypertropia in downgaze.

During this procedure, the adjacent inferior rectus muscle is poorly visualized as it passes superior to the inferior oblique muscle within Lockwood's ligament.13 In our patients, the tissue contained within the proximal hemostat probably included the lateral portion of the inferior rectus muscle that is located within Lockwood's ligament and poorly visible to the surgeon. Depending on the width of inferior rectus muscle clamped and excised, variable degrees of inferior rectus palsy would result.

von Noorden and Hansell have reported satisfactory surgical results following inferior rectus resection alone or in combination with superior rectus recession in the treatment of inferior rectus palsy.1 Despite previous mechanical injury to the inferior rectus muscle, we were able to perform inferior rectus resections in both patients. In the first patient, inferior rectus resection combined with ipsilateral superior rectus recession restored ocular alignment in primary gaze and downgaze and produced resolution of diplopia. In our second patient, an inferior rectus resection alone restored ocular alignment, with residual vertical diplopia only in extreme positions of upgaze and downgaze. Since the initial injury in our two patients most likely involved the segment of the inferior rectus muscle contained within Lockwood's ligament, the transected portions of the muscle were probably held in close apposition by their abundant fasciai attachments, making inferior rectus resection a safe procedure.

FIGURE 4: Case 1: Postoperative field measurements.

FIGURE 4: Case 1: Postoperative field measurements.

FIGURE 5: Case 2: Preoperative field measurements.

FIGURE 5: Case 2: Preoperative field measurements.

REFERENCES

1. von Noorden GK, Hansell R. Clinical characteristics and treatment of isolated inferior rectus palsy. Ophthalmology. 1991;98:253-257.

2. Van Dalen JTW, Van Mourik-Noodernbos AM. Isolated inferior rectus paresis: a report of six cases. Neuro-ophthalmology. 1984;4:89-94.

3. Roper-Hall G, Burde RM. Inferior rectus palsies as a manifestation of atypical IIIrd crania) nerve disease. American Orthoptic Journal. 1975;25:122-130.

4. Pusateri TJ, Sedwick LA, Margo CE. Isolated inferior rectus muscle palsy from a solitary metastasis to the oculomotor nucleus. Arch Ophthalmol. 1987; 105:675-677.

5. Warren W, Burde RM, Klingele TG, et al. Atypical oculomotor paresis. J Clin Neuro Ophthalmol. 1982;2:13-18.

6. Smith JL. The "nuclear third" question. J Clin Neuro Ophthalmol. 1982;2:61-63.

7. Moster ML, Schatz NJ, Savino PJ, et al. Alternating skew on lateral gaze (bilateral abducting hypertropia). Ann Neurol. 1988;23:190-192.

8. Cleary PE. Ocular manifestations of myasthenia gravis. British Orthoptic Journal. 1973;30:38-51.

9. Spoor TC, Shippman S. Myasthenia gravis presenting as an isolated inferior rectus paresis. Ophthalmology 1 979 ;86:2 158-2 160.

10. Kushner BJ. Paresis and restriction of the inferior rectus muscle after orbital floor fracture. Am J Ophthalmol. 1982;94:81-86.

11. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology. 1991;98:247-252.

12. Kuncl RW, Pestronk A, Drachman DB, et al. The pathophysiology of peni cil lamine-in duced myasthenia gravis. Ann Neurol. 1986;20:740744.

13. von Noorden GK. Binocular Vision and Ocular Motility: Theory and Management of Strabismus. 3rd ed. St Louis, Mo: CV Mosby; 1985: 49-50.

10.3928/0191-3913-19920301-12

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