Journal of Pediatric Ophthalmology and Strabismus

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Bilateral Consecutive Superior Oblique Palsy Following Fronto-Ethmoidal Sinusitis

C J Lyons, FRCS; J P Lee, FRCS, MRCP

Abstract

ABSTRACT

A 61-year-old woman developed a left superior oblique palsy as a result of frontoethmoidal sinusitis. After stabilization, the left inferior oblique and right inferior rectus were recessed. Three years later, she developed a right superior oblique palsy associated with frontoethmoiditis. The right inferior oblique and left inferior rectus were recessed.

Abstract

ABSTRACT

A 61-year-old woman developed a left superior oblique palsy as a result of frontoethmoidal sinusitis. After stabilization, the left inferior oblique and right inferior rectus were recessed. Three years later, she developed a right superior oblique palsy associated with frontoethmoiditis. The right inferior oblique and left inferior rectus were recessed.

CASE REPORT

In October 1981, a 61-year-old white British woman saw her general practitioner with a 5-month history of a persistently discharging lesion above the left medial canthus. This would heal up with crusting and break down again after 6 weeks or so. She had also noticed double vision when looking to the right. She was referred to her local hospital where a diagnosis of left medial canthal basal cell carcinoma was made on clinical grounds only. No radiographic abnormality was noted and although histological confirmation was not obtained, the patient was referred to the radiotherapy department where 3600 Rads at 30 kV were administered to the left inner canthal area in four sessions over 8 days.

Following this treatment, the lesion continued to discharge intermittently. Bacteriology grew Staphylococcus aureus. She was treated with oral erythromycin and the lesion was irrigated daily. The skin surface healed, only to break down again a few weeks later when the discharge recurred.

Further examination revealed a sinus extending posteromedially and a biopsy, performed in February 1982 revealed no tumor but necrotic tissue extending to the orbital wall. In March 1982, sinus infection was noticed on a skull x-ray (Figi).

Meanwhile, the patient's vertical diplopia was controlled with a frosted lens over her left eye and she was referred for a second opinion to Moorfields Eye Hospital where she was seen in June 1982. There, a diagnosis of left superior oblique palsy was made. Lid scarring secondary to the radiotherapy and tissue biopsy was noted.

No treatment was recommended, but it was decided that the motility and lid problems should be allowed to settle prior to surgical intervention.

In November 1982, she underwent a left frontoethmoidectomy with drainage. Biopsies were taken of the sinus which revealed granulation tissue but no tumor.

Three months later she was reviewed at Moorfields and a 4 D base-down prism was fitted to the left lens of her glasses as a temporary solution to her left hypertropia.

By October 1983, her muscle balance was stable and she underwent a right inferior rectus recession of 2 mm with a left inferior oblique recession (Figs 2-3). Postoperatively, the patient was asymptomatic apart from diplopia in extreme dextroelevation. She was followed up at sixmonthly intervals and her muscle balance appeared stable.

A year later, in December 1984, she noticed a sudden onset of vertical and torsional diplopia, this time maximal in left gaze, associated with swelling, discharge and abscess-like lesions above the right medial canthus. Later that month, she underwent a right fronto-ethmoidectomy and she was once again reviewed at Moorfields Eye Hospital. There, a right superior oblique palsy was diagnosed and the right lens of her spectacles was frosted to relieve her diplopia.

By September 1985, her muscle balance appeared stable and the right inferior oblique was recessed in combination with a left inferior rectus recession of 4 mm on an adjustable suture (Figs 4-5).

At follow-up, the patient was free of diplopia with a small left hyperphoria which gradually increased and is now well controlled with a 6 D base-down prism in her left bifocal segment.

DISCUSSION

Although superior oblique palsy is known to be a complication of sinus inflammation, there is no recent literature relating to this subject, possibly because its frequency has decreased since the advent of antibiotics.

Of the extraocular muscles, only the superior oblique is supplied on its orbital surface. The trochlear nerve enters the muscle at the junction of its middle and posterior thirds via three or four twigs. There, it is in contact with the periorbital membrane. The bony lamina which separates the frontal sinus from the orbit is often less than 0.5 mm thick.

FIGURE 1 : An anteroposterior skull X-ray showing extensive sinus opacity due to fronto-ethmoidal and maxillary sinusitis.

FIGURE 1 : An anteroposterior skull X-ray showing extensive sinus opacity due to fronto-ethmoidal and maxillary sinusitis.

FIGURE 2: Preoperative Hess chart showing marked left superior oblique underaction (and overaction of the contralateral synergists).

FIGURE 2: Preoperative Hess chart showing marked left superior oblique underaction (and overaction of the contralateral synergists).

Examination of ten skulls in the anatomy room, with transillumination of the frontal sinuses by bright glabellar illumination revealed that the posterior extent of these sinuses is variable, sometimes extending as little as 17 mm into the orbit. However in five orbits examined, the frontal sinus extended back beyond the junction of the posterior and middle thirds of the superior oblique muscle as measured from orbital apex to trochlear fossa. Microbiological study of the discharge from the patient's left sinus revealed S. aureus to be the causative organism. This species is capable of producing numerous enzymes and toxins, notably coagulase which is a thrombin-like enzyme that causes clotting of plasma, staphylokinase which converts blood plasminogen into the proteolytic enzyme plasmin, facilitating spread of the organism through tissues, and alpha toxin which is a potent vasoconstrictor. Damage to the trochlear nerves from a neighboring sinus infection is therefore consistent with the regional anatomy and with the characteristics of the organism involved which is capable of extensive tissue spread and of giving rise to microvascular thrombosis and infarction.

FIGURE 3: Postoperative Hess chart (October 1983) showing correction of the preoperative incomitance.

FIGURE 3: Postoperative Hess chart (October 1983) showing correction of the preoperative incomitance.

FIGURE 4: Preoperative Hess chart (September 1985) showing right superior oblique underaction and contralateral synergist overaction.

FIGURE 4: Preoperative Hess chart (September 1985) showing right superior oblique underaction and contralateral synergist overaction.

FIGURE 5: Postoperative Hess chart showing correction of the preoperative incomitance.

FIGURE 5: Postoperative Hess chart showing correction of the preoperative incomitance.

Superior oblique palsies are also known to result from sinus surgery.1 In this case however, diplopia preceded the surgery on both occasions.

Radiotherapy could also in principle give rise to a IVth nerve palsy. However, the x-rays used were of low penetrance and would, if anything have given rise to a Brown's syndrome secondary to reactive fibrosis around the trochlea, which was clearly not the case. Clark2 has reported a case of Brown's syndrome resulting from frontal sinusitis.

This report documents a case of bilateral consecutive superior oblique palsy arising as a result of frontoethmoidal sinusitis and the surgical management of bilateral IVth nerve palsies. It also serves to remind us of the risk of proceeding with radiotherapy without a histopathological diagnosis.

REFERENCES

1. Rosenbaum AL, Astle WF. Superior oblique and inferior rectus muscle injury following frontal and intranasal, sinus surgery. J Pediatr Ophthalmol Strabismus. 1985;22:194.

2. Clark E. A case of apparent intermittent overaction of the left superior oblique. British Orthoptic Journal. 1966;23:116-117.

10.3928/0191-3913-19900901-04

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