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Show Journal of Clinical Neuro-ophthalmology 7(1): 20-22, 1987. Fourth Cranial Nerve Palsy Following Spinal Anesthesia A Case Report Robert A. King, M.D. and Joseph H. Calhoun, M.D. © 1987 Raven Press, New York Fourth nerve palsy has been rarely seen following lumbar puncture, myelogram, or spinal anesthesia. We report a case of 4th nerve and 6th nerve palsies following spinal anesthesia. The 4th nerve palsy was best detected by using a Maddox rod. If all 6th nerve palsies occurring after spinal anesthesia were examined with a Maddox rod, more cyclovertical palsies might be discovered. Key Words: Fourth nerve palsy-Sixth nerve palsySpinal anesthesia-Maddox rod. From the Department of Pediatric Ophthalmology, Wills Eye Hospital, Philadelphia, Pennsylvania 19107. This work made possible in part by a grant from Fight for Sight, Inc., New York, to the Fight for Sight Children's Eye Center of the Wills Eye Hospital, Philadelphia, Pennsylvania. Address correspondence and reprint requests to Robert A. King, M.D., 1010 E. 19th Ave., Tammen Hall, Suite 406, Children's Hospital, Denver, Colorado 80218, U.S.A. 20 Sixth cranial nerve palsy has been described after lumbar puncture, myelogram, and following spinal anesthesia. The entity of 4th cranial nerve palsy following spinal anesthesia has been extremely rare (1-5), and to our knowledge no cases have been reported since Parks standardized the diagnosis of cydovertical palsy with the three-step test in 1958 (6). We herein describe a case of concomitant 4th and 6th nerve palsy following spinal anesthesia. CASE REPORT JG is a 33-year-old female who on July 4, 1984 underwent an uneventful Cesarean section under spinal anesthesia with pontocaine and dextrose. Beginning on the 2nd postoperative day, when she stood up, she noted a severe headache that lasted 5 or 6 days. On day 6 or 7 she noted the onset of gradually worsening diplopia, which reached its full extent on day 8. The diplopia was thought to be caused by a right 6th nerve palsy. An epidural saline patch over the area of lumbar puncture failed to cure the diplopia. A neurological evaluation confirmed the isolated 6th nerve palsy. Computed tomography with and without contrast was normal. Over the next 3 months, the right lateral rectus weakness began to improve, and it probably resolved during this time. By 4 months the diplopia was stable. Three diopter base out prisms in her glasses failed to help her symptoms, and she continued to complain of diplopia and asthenopia until she was seen at Wills Eye Hospital 13 months later. She had a 2 prism diopter right hypertropia in primary position that increased to 5 prism diopters right hypertropia on left gaze and 8 prism diopters on right head tilt. The right hypertropia measured 3 prism diopters on left head tilt. This was most easily measured R. A. KING AND ]. H. CALHOUN 21 using a Maddox rod, and, in fact, the deviation in primary position was missed prior to using the Maddox rod. She had a 5° right excyclotorsion with double Maddox rod. There was no horizontal deviation in any position of gaze, and horizontal rotation was normal. The right inferior oblique was moderately overacting, and the right superior oblique rotation was normal. The vertical fusional amplitudes measured 3 prism diopters. The diagnosis of right 4th nerve palsy was made. Her 6th nerve palsy had resolved. She was treated with 2 prism diopter base down in her right lens which gave her single vision except beyond 20° to the left. The prism relieved most of her asthenopic symptoms. She was last seen in September 1986 where her deviation in primary position had increased to 5 prism diopters of right hypertropia. Old pictures failed to reveal any long-standing head tilt. DISCUSSION Palsies of all cranial nerves, except cranial nerves 1, 9, and 10 have been described following spinal anesthesia (1), but unilateral and bilateral 6th nerve palsies are the most common after spinal anesthesia, after myelogram, and following lumbar puncture (with or without increased intracranial pressure) (7-9). The overall incidence of 6th nerve palsy following spinal anesthesia or lumbar puncture may be as high as 1 in 400 (1). Kestenbaum (10) emphasized the delayed appearance of the palsy, usually occurring 4-14 days after lumbar puncture. The typical course is one of resolution over 4-6 weeks (7,9,10). Several cases of 6th nerve palsy occurring after spinal anesthesia have taken much longer to resolve, and some cases may become permanent (3). It has been suggested that when the subarachnoid space is decompressed with a spinal needle, the abducens nerve becomes compressed between the basilar artery and the posterior cerebral artery or is stretched along the sharp edge of the petrous bone as a result of sudden production of a high intracranial pressure state, relative to the spinal pressure. It seems doubtful that toxic effects of an anesthetic agent would cause such isolated paralysis (7). We have found references linking spinal anesthesia and 4th cranial nerve palsy to be rare (1-5), and they are not included in the larger reviews detailing causes of 3rd, 4th, and 6th cranial nerve palsies (11-15). Yet it seems likely that our patient sustained a 4th and 6th cranial nerve palsy 6 or 7 days after spinal anesthesia for a Cesarean section. JClin Neuro-ophthalmol, Vol. 7, No.1, 1987 In reviewing 324 cases of cranial nerve palsy follOWing spinal anesthesia, Thorsen (1) noted 299 cases of 6th nerve palsy alone and in 8 cases another cranial nerve injury along with the 6th. He cited two 4th nerve palsies occurring alone and three accompanying the 6th and other cranial nerves, but he did not comment on how the diagnosis was made. Levine reported a case of complete ophthalmoplegia (3). Fourth cranial nerve palsies can be acquired or can be decompensated congenital 4th nerve palsies. The difference can be difficult to distinguish. Characteristically the congenital variety has larger fusional amplitudes, larger hypertropia, and comparatively less torsional deviation. The ratio of hypertropia to cyclotorsion in congenital 4th nerve palsies is much higher than in acquired 4th nerve palsy. Dickson and Calhoun made such a comparison between six patients with congenital and six patients with acquired 4th nerve palsies (16). The average ratio of hypertropia to excyclotorsion measured greater than 4 in the former and just over 1 in the latter. Our patient had a small hypertropia, small fusional amplitudes, and a comparatively large amount of excyclotorsion (a ratio of 0.4). She almost certainly had an acquired 4th nerve palsy. Our case was typical in its delayed onset and its resolution of the 6th nerve component, probably within 3 months of onset. The 4th nerve palsy was not identified until 13 months after onset, but it probably caused the complaints of diplopia that were so recalcitrant to treatment with horizontal prism. Trochlear nerve involvement after spinal anesthesia is rare. Its continuation past 3 months makes it different from the course of abducens palsy after spinal anesthesia, which generally clears in a matter of weeks. The pathophysiology of this cranial nerve palsy is probably similar to the proposed mechanism of 6th nerve palsy where the low-pressure state in the subarachnoid space causes compression of the nerve between brain substance and vessel or bone. The 4th nerve could be compressed anywhere along its lengthy course after exiting from the posterior brainstern until it pierces the dura, thereby leaving the subarachnoid space. In trauma, the 4th nerve is thought to be particularly vulnerable as it leaves the dorsal brainstem. Compression of the brainstem against the tentorium or compression of the cerebellum against the floor of the posterior fossa may cause the nerve palsy (7). Toxic effects of the anesthetic agent or transitory meningeal inflammation have been postulated as causing nerve palsies after spinal anesthesia (3), 22 FOURTH CRANIAL NERVE PALSY but these mechanisms do not explain the relative selectiveness of postspinal anesthesia nerve palsies. The common event linking spinal anesthesia, lumbar puncture, and myelography (9) is the decompression of the subarachnoid space by the spinal needle or needle tract, and this decompression and resulting pressure on the nerve seems to us to be the inciting cause of nerve damage. Finally, perhaps 4th nerve palsy is more common than the literature indicates. If there were a transient palsy of the trochlear nerve along with the abducens nerve, it would be masked by the large estropia. If both improved, as is the course of most nerve palsies, the diagnosis of 4th nerve palsy might never be made. Perhaps if all of these postspinal anesthesia palsies were investigated with a Maddox rod, more cyclovertical deviations would be discovered. In fact, it might be common. In the case reported here, the hypertropia in primary position was difficult to see despite the patient's complaints of diplopia. Placing a Maddox rod with the ridges oriented vertically made the diagnosis easier. A simultaneous 4th nerve and 6th nerve palsy should be suspected when the patient has diplopia even out of the field of action of the lateral rectus muscle and when the diplopia changes from horizontal to vertical in the adducting field. Management of acquired 4th nerve palsy is limited to patching to relieve diplopia, prism glasses, and surgery. As in other extraocular muscle palsies, no surgery should be performed prior to stabilization of the tropia, certainly not before 6-12 months. Small hyperdeviations can probably be managed successfully with prisms, especially if there is some comitance of the deviation and a large field of comfortable binocular vision can be obtained. Surgery should be reserved for larger deviations and incomitant deviations where little or no field of single binocular vision can be obtained with vertical prisms or in case of symptomatic torsional deviation. Surgery would most commonly involve strengthening the affected superior oblique tendon, recessing its antagonist (the infe-rior oblique), or recessing its yoke (the contralateral inferior rectus) for vertical imbalance. Advancing the anterior half of the superior oblique tendon (Harada-Ito) would relieve the torsional deviation, if that alone were the cause of the symptoms (17). Physicians should be aware that not only 6th cranial nerve palsy but also 4th cranial nerve palsy can be seen following spinal anesthesia. REFERENCES 1. Thorsen G. Neurological complications after spinal anesthesia. Acta Chirg Scand 1947;95(Suppl 121):75-94. 2. Shapira TM, Schall 5, Rodin M. Total unilateral ophthalmoplegia follOWing spinal anesthesia. Am I Ophthalmol 1950;33:970-2. 3. Levine J. Paralysis of an extraocular muscle after spinal anesthesia. Arch OphthalmoI1930;4:516-20. 4. Biggam MJ: Paralysis of ocular muscles following spinal anesthesia. Br JOphthalmoI1932;16:552-4. 5. Mansour AM, Reinecke RD. Central trochlear palsy. Survey OphthalmoI1986;30(5):279-97. 6. Parks MM. Isolated cyclovertical muscle palsy. Arch OphthalmoI1958; 60:1027-35. 7. Miller NR: Walsh and Hoyt's clinical neuro-ophthalmology, 3rd edition, Baltimore: Williams & Wilkins., 1985;652-784. 8. Insel TR: Abducens palsy after lumbar puncture. N Engl J Med 1980;303:703. 9. Newmark H III, Levin N, Apt RK, Wax JD. Esotropia: unusual complications of myelography and pneumoencephalography. Am JNeuroradio/1981;2:278-81. 10. Kestenbaum A: Clinical methods of neuro-ophthalmologic examination. New York: Grune & Stratten, 1961:287. 11. Rucker CW: The causes of paralysis of the third, fourth, and sixth cranial nerves. AmI Ophthalmol 1966;61:1293. 12. Rucker CW: Paralysis of the third, fourth, and sixth cranial nerves. Am JOphthalmoI1958;46:787. 13. Rush JA, Younge BR. Paralysis of cranial nerves III, IV, and VI: cause and prognosis in 1000 cases. Arch Ophthalmol 1981;99:76. 14. Harley RD: Paralytic strabismus in children: etiology incidence and management of the third, fourth and sixth nerve palsies. Ophthalmology 1980;85:24. 15. Coppeto JR, Lessell 5: Cryptogenic unilateral paralysis of the superior oblique muscle. Arch OphthalmoI1978;96:275. 16. Dickson JB, Calhoun JH: Differences between congenital and acquired superior oblique palsies. In Reinecke RD ed. Strabismus II, New York: Grune & Stratten, 1984:815-9. 17. Troia RN, Nelson LB, Calhoun JH, Harley RD: Surgical correction of excyclotropia. Am Orthoptic J1985;35:63-7. JClin Neuro-ophthalmol, Vol. 7, No.1, 1987 |
