| OCR Text |
Show Journal of Clillical N"lIro-ol'lJIlrllllllology 6121: 91-95, 1986. Bilateral Sixth Nerve Pareses with Temporal Arteritis and Diabetes Walter M. Jay, M.D., and Sarkis M. Nazarian, M.D. ,. 19H6 Raven Press, New York A 78-year-old white woman presented with a I-month history of neck and right shoulder pain and a I2-day history of acute horizontal diplopia. On examination, bilateral sixth nerve pareses were present, right greater than left. On evaluation, the patient was noted to have normal fasting blood sugars, but moderately elevated blood sugars after a glucose load. A temporal artery biopsy was performed which was positive. Whether diabetic or arteritic, bilateral sixth nerve pareses resulted in our patient seeking medical attention. By considering temporal arteritis, it is possible that blindness was avoided. From the Departments of Ophthalmology (W.M.J.) and Neurology (S.M.N.), University of Arkansas for Medical Sciences, and the John L. McCleIlan Veterans' Hospital (S.M.N.), Little Rock, Arkansas. Address correspondence and reprint requests to W. M. Jay, M.D., Department of Ophthalmology, University of Arkansas for Medical Sciences, Mail Slot #523,4301 W. Markham, Little Rock, AR 72205, U.S.A. 9/ Temporal arteritis is a generalized systemic disease with many manifestations (1-9). The most serious neuro-ophthalmologic complication is unilateral or bilateral blindness. Often, unfortunately, this is the presenting complaint. Another neuroophthalmologic complication that may occur in temporal arteritis prior to visual loss is that of diplopia. Diplopia has been described as occurring in 2-43% of patients with temporal arteritis (10). In the present case report, we describe a 78-year-old white woman with bilateral sixth nerve pareses who had diabetes and biopsy-proven temporal arteritis. By appropriate administration of systemic steroids, visual loss was avoided. CASE REPORT L.S., a 78-year-old white woman, was referred to the University of Arkansas Hospital with a 1month history of neck and right shoulder pain and a 12-day history of acute horizontal diplopia. Since the onset of neck pain, the patient experienced generalized malaise and poor appetite. The pain was not aggravated by neck motion and did not radiate into the right arm. While speaking on the phone 2 weeks after developing neck pain, she noted sudden onset of painless, horizontal diplopia. She noted no other visual changes. She had mild hypertension and a partial colectomy for adenocarcinoma 15 years previously. She was on a thiazide diuretic. The patient was seen initially by her family physician who noted bilateral sixth nerve pareses. She had a computed tomographic (CT) scan of the head, which revealed mild cortical atrophy. Electroencephalogram showed mild left temporal slowing. Bone scan was normal. A random blood sugar was 171 mg/dl, and Wintrobe sedimentation rate was 45. Glucose tolerance test gave values of 185, 192, and 186 mg/dl at 0.5, 1, and 2 h, respectively. The fasting glucose was 90 mg/dl, and all 92 W. M. JAY AND S. M. NAZARIAN the urine sugars were negative, except a 2+ reaction at 2 h. At this point, she was referred to the University of Arkansas Medical Center for further evaluation. On admission, blood pressure was 150/80. Moderate to severe posterior neck and occipitotemporal tenderness was present bilaterally. The neck was supple, the carotid pulses full and free of bruits. Cardiac and pulmonary exam was normal. A colostomy was present. Abdomen and extremities were otherwise normal. Visual acuity was 20/40 and color vision was normal in both eyes. Goldmann visual fields were normal. Extraocular motility was remarkable for bilateral sixth nerve pareses, more pronounced on the right (Fig. 1). Forced ductions were negative. Specifically, both eyes could be turned out readily into full abduction. Vertical movements were normal. No nystagmus was present. Pupils were 3 mm in diameter and briskly reactive. There was no ptosis or proptosis, and eyelid closure was normal. Slit lamp biomicroscopy revealed mild to moderate nuclear sclerotic lens changes consistent with the patient's vision. Corneal sensation was normal. Applanation tonometry was 17 in both eyes. Ophthalmoscopic exam was normal, with cup-to-disc ratios of 0.4 in both eyes. Neurologic exam revealed normal mentation and fluent speech. Cranial nerves VII through XII were normal. On general motor exam, there was proximal right upper extremity weakness due to shoulder pain. Dexterity and coordination were normal. Gait was slightly wide-based. On sensory exam, there was slightly diminished pain sensation in right second cervical dermatome distribution. Complete blood count revealed a hemoglobin of 12.4 gldl, and a white cell count of 9,OOO/ml. Wintrobe sedimentation rate was 49. Electrolytes were normal, and fasting glucose was 107 mgldl. Urinalysis was normal, except for 2 + glucose reaction. Cervical spine radiographs showed mild degenerative changes in the fifth and sixth vertebrae. A CT scan of the head, with special attention to the orbits, sella turcica, and cavernous sinus region, was performed (Figs. 2 and 3). A Tensilon test was negative. A lumbar puncture was performed, with an opening pressure of 12 cm of water. Protein was 25 mg/dl and glucose was 62 mgldl. One red and one nucleated cell were seen per high-power field. The differential was 85% lymphocytes, 8% monocytes, and 7% histiocytes. Cytologic examination was normal. VDRL was negative. Because of a clinical suspicion of temporal arteritis, the patient was started on prednisone 60 mg daily. A temporal artery biopsy was performed 2 days later, and a 3.7 cm long section of a 4 mm diameter, tortuous artery was excised. Multiple histologic sections showed an inflammatory infil- FIG, 1,. Composite p~otogr~p.h showing eye movements in nine positions of gaze Note bIlateral abductIon defICit present. . I Clin Neuro-ormlhalmol. Vol. 6. No.2. 1986 BILATERAL SIXTH NERVE PARESES 93 (.) (b) FIG. 2. (a,b) Axial CT scans showing extraocular muscles. bate (Fig. 4). Large cells suggestive of giant cells were seen (Fig. 5). The patient's neck and shoulder pain, as well as her generalized malaise, rapidly resolved, although her bilateral sixth nerve pareses did not change. Fasting blood sugar was 95 mg/dl. She was discharged on prednisone 60 mg every day. Follow-up visit 3 weeks after discharge revealed that she was free of pain, but she continued to exhibit bilateral sixth nerve pareses. Westergren sedimentation rate was 17. Fasting blood sugar was 100 mg/dl. Her prednisone dose was lowered to 40 mg daily. At 8 weeks after discharge, diplopia was still present. The bilateral sixth nerve pareses im- FIG. 3. (a,b) Coronal CT scans showing extraocular muscles. 1eli" N~uro-ophtht"mol. Vol. 6. No.2. 1986 94 W. M.IAY AND S. M. NAZARIAN AG.4. Temporal artery biopsy. Note segmental disruption of internal elastic lamina and inflammatory infiltrate. ( x 32.) proved, with only minimal limitation still present, right more than left. Clinically, saccadic velocities on abduction were slow. Westergren sedimentation rate was 18. At this point, her prednisone dose was lowered to 30 mg daily. At 11 weeks after discharge (96 days after the diplopia appeared), the patient continued to have double vision. Saccadic velocities on abduction remained - f1'G. 5. Temporal artery biopsy. Note presence of giant cell. (x 80.) I Cli/l Nfll""ovhlhalmol. Vol. 6. No.2. 1986 BILATERAL SIXTH NERVE PARESES 95 slow bilaterally. Westergren sedimentation rate was 7. Her prednisone dose was lowered to 20 mg daily. DISCUSSION Barricks et al. presented a histopathologic study of an 80-year-old man with temporal arteritis who had bilateral visual loss and ophthalmoplegia (11). Their study supported the view that the lesions causing the ophthalmoplegia were within the orbit. Ischemic necrosis of the extraocular muscles appeared to be the major feature. One could question whether nerve or muscle balance involvement was responsible for the diplopia our patient experienced. In our opinion, nerve involvement was more likely. First, there was no conjunctival injection to suggest extraocular muscle inflammation. Second, forced duction testing did not reveal restrictive myopathy. Finally, high-resolution orbital CT scanning failed to reveal extraocular muscle pathology. C. M. Fisher has described previously a patient with bilateral "sixth nerve palsies" (12). His case differs from the present case in three important respects. First, besides the bilateral "sixth nerve palsies," there was also involvement of the "left third nerve." Secondly, in Fisher's patient, the palsies lasted less than a week, compared to over 3 months in our patient. Finally, the diagnosis of temporal arteritis was made prior to the loss of vision in our patient. Reports, such as that by Fisher, have been invaluable in allowing us now to make the diagnosis of temporal arteritis prior to visual loss. Meadows also has reported one case of bilateral abduction deficits in his series of 80 patients with temporal arteritis (13). Our patient also had evidence of carbohydrate intolerance. She had two urine specimens that were 2+ reactive for glucose. Further, her glucose tolerance test revealed moderately elevated blood sugars. However, all her fasting blood sugars were normal, including those while on prednisone therapy. Controversy exists in the endocrinologic literature on whether or not our patient should be classified as diabetic (14,15). Clearly, there is sufficient evidence to indicate that a carbohydrate intolerance is present. Thiazide diuretics are known to interfere with carbohydrate metabolism (16,17). In one study, 30% of hypertensive patients in thiazide diuretics had abnormal glucose tolerance (18). Our patient was hypertensive and was receiving long-term thiazide therapy. Her use of this medication may have contributed to her carbohydrate intolerance. The question arises whether the bilateral sixth nerve pareses present in our patient are diabetic in origin (19). This possibility cannot be ruled out. There appears to be no correlation between severity of glucose metabolism defect and occurrence of cranial nerve palsies (20). In Keane's series of 125 cases of bilateral sixth nerve palsy, none were classified as diabetic in origin (21). Whether diabetic or arteritic, the bilateral sixth nerve pareses resulted in our patient seeking medical attention. By considering temporal arteritis, it is possible that blindness was avoided in this patient. REFERENCES 1. Keltner J. L.: Giant-cell arteritis. Ophthalmology 1982;89:1101-10. 2. Healey L. A., Wilske K. R.: Manifestations of giant cell arteritis. Med Clin North Am 1977;61:261-70. 3. Huston K. A., Hunder G. G., Lie J. T., Kennedy R. H., Elveback L. R.: Temporal arteritis: a 25-year epidemiologic, clinicaL and pathologic study. Ann Intern Med 1978;88: 162-7. 4. Hollenhorst R. W., Brown J. R., Wagener H. P., Shick R. M.: Neurologic aspects of temporal arteritis. Neurology 1960;10:490-8. 5. Dimant J., Grob D., Brunner N. G.: Ophthalmoplegia, ptosis, and miosis in temporal arteritis. Neurology 1980;30:1054-8. 6. Cohen O. N., Damaske M. N.: Temporal arteritis: a spectrum of ophthalmic complications. Ann Ophthalmol 1975;7:1045-54. 7. Goldberg R. T.: Ocular muscle paresis and cranial arteritis -an unusual case. Ann Ophthalmol 1983;15:240-3. 8. Cullen J. F., Coleiro J. A.: Ophthalmic complications of giant cell arteritis. SUYL' Ophthalmol 1976;20:247-60. 9. Wang F. M., Henkind P.: Visual system involvement in giant cell (temporal) arteritis. Sur" Ophthalmol 1979;23:26471. 10. Goodman B. W.: Temporal arteritis. Am I Med 1979;67:83952. 11. Barricks M. E., Traviesa D. B., Glaser J. 5., Levy I. 5.: Ophthalmoplegia in cranial arteritis. Brain 1977;100:20921. 12. Fisher C M.: Ocular palsy in temporal arteritis. MimI Med 1959;42:1258-68. 13. Meadows S. P.: Temporal or giant cell arteritis. Proc R Soc Med 1966;59:329-33. 14. McDonald G. W., Fisher G. F., Burnham C: Reproducibility of the oral glucose tolerance test. Diabetes 1965;14:473-80. 15. Hayner N. 5., Kjelsberg M. 0., Epstein F. H., Francis T.: Carbohydrate tolerance and diabetes in a total community, Tecumseh, Michigan. 1. Effects of age, sex, and test conditions on one-hour glucose tolerance in adults. Diabetes 1965;14:413-23. 16. Wilkins R. W.: New drugs for the treatment of hypertension. Ann Intern Med 1959;50:1-10. 17. Schwab R. H., Perloff J. K., Porus R. L.: Chlorothiazideinduced gout and diabetes. Arch Intern Med 1963;111:46570. 18. Breckenridge A., Welborn T. A., Dollery CT., Fraser R.: Glucose tolerance in hypertensive patients on long-term diuretic therapy. Lancet 1967;1:61-71. 19. Rush J. A.: Extraocular muscle palsies in diabetes mellitus. lilt Opllthalmol Clill 1984;24(4):155-9. 20. Glaser J. 5.: Neuro-ophthalmology. Hagerstown: Harper and Row, 1978:250. 21. Keane J. R.: Bilateral sixth nerve palsy: analysis of 125 cases. Arch Neurol 1976;33:681-3. , Gill Neuro-ovlttlmlmol, Vol. 6, No.2. 1986 |
