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Show Journal 01 CllIlleal NCllro- ophthalmology 12( 2): 85- 87, 1992. Combined Third and Sixth Nerve Paresis Following Optic Nerve Sheath Fenestration Kyle H. Smith, M. D., J. Terry Wilkinson, M. D., and Glen O. Brindley, M. D. '~ 1992 Raven Press, Ltd., New York The authors report a case of transient third and sixth nerve paresis as a complication of optic nerve sheath fenestration in a patient with pseudotumor cerebri. The motility and pupillary abnormalities that are commonly associated with this procedure are reviewed briefly. Key Words: Third nerve paresis- Sixth nerve paresisOptic nerve sheath fenestration- Pseudotumor cerebri. From the Divisions of Ophthalmology ( K. H. S. and G. O. B.) and Neurology a. T. W.), Scott & White Clinic, Temple, Texas, U. S. A. Address correspondence and reprint requests to Dr. Scott & White Clinic, 2401 South 31st Street, Temple, TX 76508, U. s. A. 85 Optic nerve sheath fenestration is gaining acceptance as the surgical procedure of choice for the management of pseudotumor cerebri associated with progressive loss of vision or visual field ( 1,2). Recent studies have also demonstrated a possible role for this procedure in the treatment of the progressive form of ischemic optic neuropathy ( 3- 5). The most frequently reported surgical complications are transient motility disturbances and tonic pupils ( 6- 12). In this article, we describe a patient with pseudotumor cerebri who developed a complete third and partial sixth nerve paresis following optic nerve sheath fenestration. To our knowledge this is the first report of a multiple cranial neuropathy as a complication of this procedure. CASE REPORT A 34- year- old obese white woman presented with a 4- month history of frontal headache and transient obscurations of vision. Her visual acuity was 20/ 20 au. Automated visual fields demonstrated bilateral generalized construction with enlarged blind spots. Funduscopic examination revealed fully developed papilledema au. A magnetic resonance imaging ( MRI) scan of the head with gadolinium showed no significant abnormality. A diagnosis of pseudotumor cerebri was made after a lumbar puncture yielded normal cerebrospinal fluid ( CSF) with an opening pressure of 330 mm H2 0. The patient was started on Diamox 500 mg three times a day. Three weeks later her headaches persisted unchanged, and repeat lumbar puncture yielded an opening pressure of 470 mm H20. Repeat visual fields revealed definite progression of the generalized constriction. Her visual acuity remained 20/ 20 au. Because of her progressive field loss with con- 86 K. H. SMITH ET AL. tinued headaches and high CSF pressure despite medical therapy, an optic nerve sheath fenestration under general anesthesia was performed on the left by the medial approach as described by Sergott et al. ( 12). Optic nerve sheath exposure was initiated by rotation of the globe laterally with the superior and inferior rectus traction sutures. The section of nerve sheath approximately 3 to 7 mm behind the globe was then visualized by careful retraction of orbital contents with small malleable retractors and cotton- tipped applicators. At no time did the surgeons feel that the retractors were inadvertently placed too deeply within the orbit. No significant bleeding was observed, so no cautery or compression was required for hemostasis. Multiple longitudinal incisions were made in the nerve sheath without difficulty. Only a small amount of CSF was released from the subarachnoid space as compared to other similar procedures in our experience. The medial rectus was reattached with standard technique. Throughout the procedure vital signs were closely monitored by an anesthesiologist who noted no significant fluctuations in blood pressure. On the first postoperative day a complete leftsided ptosis was evident. The pupil was dilated and nonreactive, and ocular motility was virtually nil. There was no evidence of retrobulbar hemorrhage. One week postop, after the conjunctival edema had resolved, a third nerve paresis was present as evidenced by a complete ptosis, absent adduction and elevation, and impaired depression. The pupil remained fixed and dilated. In addition, there was limited ability to abduct the eye, indicating a probable concomitant partial sixth nerve paresis. Fourth nerve function was judged to be intact as evidenced by retained depression of the globe with incyclotorsion. Two weeks postop her third and sixth nerve paresis persisted, but the papilledema was resolving, and the CSF opening pressure had decreased to 310 mm H20. She remained on oral Diamox throughout the postoperative course because of persistent, although improved, headaches. The ptosis and ocular motility began to improve during the third postoperative week. After 3 months the motility disturbance had almost totally resolved, with persistent diplopia only in extreme right gaze. A faint residual ptosis was also noted. No aberrant regeneration was detected. Her headaches were much improved, the papilledema had completely resolved bilaterally, and the visual fields had returned to normal. The pupil remained dilated with only minimal sectoral response to light. Her vision remained 20/ 20 OU throughout. JClm Ncu,,'- uphilu; u".,., V/ 12 No. 2. 1992 COMMENT Optic nerve sheath fenestration appears t? be quite effective in reversing papilled~ maand VIsual field defects in pseudotumor cerebn, although the mechanism of action remains controversial ( 1). The surgical complications are, in general, infrequent and of minor significance. Since 1973 six different series ( 6- 9,11,12) have reported on a total of 115 optic nerve sheath decompressions ( 86 patients) for pseudotumor cerebri. Minor motility disturbances, including one transient sixth nerve paresis, were reported in six patients. Another series of 14 patients reported transient diplopia as a " common" complication and cited one case of transient third nerve palsy that was attributed to traction ( 10). Most of these motility disturbances are probably related to surgical manipulation of the medial rectus, which is temporarily disinserted from the globe during the procedure to provide adequate exposure to the intraconal space. Other reported complications include occasional tonic pupils, which are usually transient ( 6,8,10,11). Permanent tonic pupils were reported in 16 eyes from the early surgical experience in one series ( 7) using the lateral approach. This complication was later eliminated by a refined surgical technique with avoidance of the ciliary ganglion. Our patient is, to our knowledge, the first reported case of a concomitant third and sixth nerve paresis following optic nerve sheath fenestration. The abduction weakness could possibly be explained by a mechanical or restrictive process, rather than an actual sixth nerve paresis. However, the third nerve paresis was unequivocal. The authors had successfully performed this procedure six times previously without encountering a significant motility disturbance postoperatively. The technique employed in this case did not deviate from prior procedures. The postoperative cranial neuropathies were therefore quite unexpected. The mechanism of injury is unclear, but apparently involved both the superior and inferior divisions of the oculomotor nerve, as well as the abducens nerve. The most likely etiology seems to be an indirect insult to the nutrient vessels supplying the cranial nerves near the orbital apex. The insult may have been precipitated by intraoperative pressure or traction, although the authors noted no inordinate pressure or traction during the procedure. Fortunately, these cranial neuropathies proved to be reversible. The persistent tonic pupil is thought to be the result of direct intraoperative trauma to the posterior ciliary nerves. As a result of this unusual case, we now include a discussion COMBINED THIRD AND SIXTH NERVE PARESIS 87 of ptosis and significant motility disturbances as possible complications during the preoperative counseling of our patients anticipating this procedure. REFERENCES 1. Keltner JL. Optic nerve sheath decompression. Arch OphthalmoI1988; 106: 1365- 9. 2. Spoor TC, Ramocki JM, Madion MP, Wilkinson MJ. Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression. Am I Ophthalmol 1991; 112: 177- 85. 3. Kelman SE, Elman MJ: Optic nerve sheath decompression for nonarteritic ischemic optic neuropathy improves multiple visual function measurements. Arch Ophtlzalmol 1991; 109: 667- 71. 4. Sergott RC, Cohen MS, Bosley TM, Savino Pl. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy. Arch Ophthalmol 1989; 107: 17H- 54. 5. Spoor TC, Wilkinson M). Ramocki ) M. Optic nerve sheath decompression for the treatment of progressive nonarteritic ischemic optic neuropathy. Am JOphthalmol 1991; 111: 724- 8. 6. Brourman NO, Spoor TC, Ramocki JM. Optic nerve sheath decompression for pseudotumor cerebri. Arch Ophthalmol 1988; 106: 1378- 83. 7. Corbett J). Nerad JA, Tse DT, Anderson RL. Results of optic nerve sheath fenestration for pseudotumor cerebri. Arch OphthalmoI1988; 106: 1391- 7. 8. Galbraith ) EK, Sullivan JH. Decompression of the perioptic meninges for relief of papilledema. Am J Ophthalmol 1973; 76: 687- 92. 9. Hupp SL, Glaser JS, Frazier- Byrne S. Optic nerve sheath decompression: review of 17 cases. Arch Ophthalmol 1987; 105: 386- 9. 10. Kilpatrick C), Kaufman DV, Galbraith ) EK, King JO. Optic nerve decompression in benign intracranial hypertension. Clill Ex!, Neural 1981; 18: 161- 8. 11. Knight RSG, Fielder AR, Firth JL. Benign intracranial hypertension: visual loss and optic nerve sheath fenestration. J Neural Neurosurg Psychiatr 1986; 49: 243- 50. 12. Sergott RC, Savino P). Bosley TM. Modified optic nerve sheath decompression provides long- term visual improvement for pseudotumor cerebri. Arch Ophthalmol 1988; 106: 1384- 90. I Clill Neuro- ophtha/ mol, Vol. 12, No. 2, 1992 |
